Consistent with these findings, the depletion of IPMK in primary myocytes led to reduced AKT activation in response to insulin and IPMK-MKO mice developing glucose intolerance, which are similar to the findings in mice with an overexpression of kinase-dead insulin receptor (IR) or IGF-1 receptor (IGF1R). The gene discussed is AKT1; the disease is Glucose intolerance.