With findings of aPKC deficiencies in muscle studies, it was particularly surprising to find increases in PKC‐λ activity in livers of DIO/MetS/T2DM mice17, 20, 21, 40, 41, 42, 43, 44; and increases in activity and mRNA and protein levels of PKC‐ι, and operation of a feed‐forward, positive‐feedback, autocatalytic, mechanism, in livers of obese and T2DM humans.18, 19. This evidence concerns the gene PRKCH and type 2 diabetes mellitus.