Notably, these changes parallel those previously reported for CAV1 in human adipose tissue.58 Interestingly, there is evidence supporting that sustained activation of Akt, as occurs in 3T3‐L1 adipocytes with enhanced NECC2 expression levels, leads to a negative feedback of insulin signalling and, therefore, insulin resistance.25 Together, these and our morphological and functional data in 3T3‐L1 cells may suggest a role for NECC2 in obesity and the development of glucose metabolism derangements. The gene discussed is CAV1; the disease is obesity disorder.