The increased glucose tolerance in TMLKO mice seems to contrast with the observations in TMEM16A global knockdown mice, in which a more severe glucose intolerance, due to deficiency of insulin secretion at the early stage of HFD (5 weeks) was reported.[22] An in vitro study further suggested that TMEM16A is required for glucose‐induced insulin secretion in β cells.[21] Two factors may explain this discrepancy. This evidence concerns the gene INS and glucose measurement.