Changes in glucose tolerance were not apparent after the maintenance of mice (either male of female) on a HFD, suggesting that the phenotype might be rescued by changes in response to high-fat feeding and insulin resistance. One possible explanation might be an increase in the expression of other VPS13 family members, which could be triggered by a HFD, thus compensating for the absence of VPS13C. According to a recent study of mouse islet cell transcriptomes (5), Vps13c mRNA levels are two to three times those of Vps13a, -b, and -d in the β-cell under conditions of normal feeding. Whether changes in the expression of any of these genes occur under the stress of a HFD has yet to be investigated. We note also that a recent eQTL study (9) did not report a significant association with VPS13C (or other genes at this locus) and T2D risk, although whether the latter study was adequately powered to detect small changes is uncertain.