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Overexpression of c-Kit has recently been shown to ameliorate beta cell function by increasing the beta cell mass and insulin secretion, thus counteracting the deleterious effects of a high-fat diet on glucose homeostasis. The c-Kit-dependent effects are due to enhanced Akt activity that phosphorylates and inhibits glycogen synthase kinase 3β (GSK3β), thereby increasing the expression of numerous genes that promote insulin production and cell proliferation. Regulating the c-Kit/Akt/GSK3β pathway may provide novel means for improving beta cell function in type 2 diabetes.

The platelet-derived growth factor (PDGF) family of tyrosine kinase receptors: a Kit to fix the beta cell?