Most importantly, insulin stimulation of muscle‐dependent glucose disposal in hyperinsulinemic‐euglycemic clamp studies was found to be impaired in T2DM humans37, 38 and monkeys,39 and, moreover, accompanied by deficiencies in both activity and amount of muscle PKC‐ι, the primate‐specific aPKC isoform (98% amino acid homology to nonprimate PKC‐λ). Here, INS is linked to type 2 diabetes mellitus.