Finally note that hepatic FoxO1 phosphorylation is constitutive when PKC‐λ/ι is deficient, as in mice with heterozygous knockout of PKC‐λ that are fully protected from developing increases in gluconeogenic and lipogenic enzymes, and, for that matter, do not develop glucose intolerance or T2DM during high‐fat‐feeding, but, on the other hand, rapidly become overtly diabetic when PKC‐λ is overexpressed specifically in liver.42 Here, PRKCH is linked to Glucose intolerance.