What data gaps, if any, need to be filled to effectively and efficiently conduct a risk assessment to address this problem formulation?

First, one must decide on the "critical effect" that is the basis of the risk assessment for multiple PFAS.
There is not a consensus between different authorities on which forms of toxicity (development, hepatotoxicity, etc.) should be the basis of the risk assessment. Without the availability of more information on specific toxic effects (e.g. mode of action for immunotoxicity), it's hard to make a judgement regarding which critical effect should form the basis of the risk assessment.

Second, once the critical effect is decided, it can be that there are missing data for some PFAS in the key studies that form the basis of the risk assessment. Therefore, the number of PFAS than can be grouped will be limited by data availability on effects. There is a severe lack of true mixture toxicity studies (i.e. when a test species is exposed to mixture of multiple PFAS simultaneously).

Third, it is uncertain how to deal with exposure to precursors (many of which are not routinely monitored or are unknown) to perfluoroalkyl acids (PFAAs) (e.g. can we assume that they will be absorbed and rapidly metabolized to PFAAs in vivo and thus adding to exposure?). Also, intermediates between the precursors and the PFAAs can also be long-lived and toxic. The detailed information on kinetics of complex transformation processes between precursors and terminal transformation products (usually PFAAs), as well as the toxicities of intermediates, are data gaps that are unlikely to be filled.

Role of precursor PFAS and their biotransformation
Toxicity of several subgroups and mode of toxicity of each subgroups
Additive nature of mixture toxicity
Extrapolation of toxicity from animal model to humans

As outlined in Round 1, the most pressing data gaps relate to toxicological mechanisms for PFAS, so that sub-groups can be constructed with the commonality that is implicit in grouping methodologies proposed in US EPA "Guidelines for health risk assessment of chemical mixtures". The basic assumption, as outlined in this document ("Since the assumption of dose addition is most properly applied to compounds that induce the same effect by similar modes of action, a separate hazard index should be generated for each end point of concern. Dose addition for dissimilar effects does not have strong scientific support, and, if done, should be justified on a case-by-case basis in terms of biological plausibility") implies that a Hazard Index calculated from the exposure/HBGV ratios for individual or grouped PFAS requires data that currently exists for only a few individual PFAS.

In vitro data on PFAS mixtures would allow evaluating the dose additivity assumption, which seems to be central to the derivation of a health-based drinking water guideline.

If the analysis plan and resources are limited to data available in October 2021, then presumably this question is meant to define areas of uncertainty. A different question is rather what information would be most valuable in producing a "better" risk assessment, one that is more precise and accurate. I think the data gap answers from the experts in Round 1 were largely directed at this latter question.

Data exist to conduct a risk assessment of the PFAS that have been measured in the UCMR3. If one wishes to expand this list, simply considering pchem properties is insufficient. This would be a rudimentary first step, and analyses would also have to include factors such as use, pathway to drinking water, and actual measurements in drinking water.

Again, grouping and potency (does response) rise to the top of the priority list. As a matter of potency, toxicokinetics should be considered, at least in rudimentary form.

Currently, data gaps exist for all of the available resources (toxicity, exposure, physical-chemical properties) for many individual PFAS. Additionally, new approach methodologies and other rapid/high-throughput methods for evaluating large numbers of PFAS are still in their infancy for PFAS. It may be possible to conduct a risk assessment on some of the well-studied PFAS (i.e., "long-chain" perfluoroalkyl acids (PFAAs) that include the perfluorocarboxylic acids (PFCAs) and perfluorosulfonic acids (PFSAs), but assumptions will still have to be made for individual PFAS within this "subgroup" that are still lacking either toxicological, exposure, or physical-chemical property data.

Strictly speaking, there are no data gaps in the problem formulation that need to be filled since as point 5 of the problem formulation states the groupings will only rely on available data. Now given the state of available data on the toxicity of PFAS it is safe to say that the decisions on groupings generated will be very uncertain and are likely to need to be revised when additional data become available. Since I am not familiar with all of the data available PFAS, I am unable to identify specific data gaps.

It will be important to know how important the drinking water pathway is relative to other routes of exposure (Required for apportionment of exposure to drinking water in setting the MCL).

Careful and sound wording is necessary to define the problem/objective and apply throughout. Limitations need to be addressed as well otherwise the different disciplines struggle with themselves and between each other.
In my view, risk assessment must be followed by risk management, which should be revisited periodically as to efficiency and be flexible for adaptations.
it would be a failure to discuss forever, rather take measures. Risk assessment alone (like environmental or biomonitoring) do not change anything