Defects in glucose transport and atypical protein kinase C (αPKC) activation were observed in cultured myocytes obtained from obese/impaired glucose tolerant humans.51 PIP3, which is a derivate of phosphatidylinositol by class I phosphoinositide 3‐kinases (PI3K) (Figure 2), is known to mediate insulin effects on glucose transport through αPKC.48 In this clinical hyperinsulinemic‐euglycemic clamp study, compared to control, insulin induced αPKC activation was diminished by decreased ability of PIP3 to directly activate αPKCs in the impaired glucose tolerance and type 2 diabetic groups. Here, INS is linked to Impaired glucose tolerance.