For example, while adipocyte-specific knockout of HDAC6 in mice causes glucose intolerance and skeletal muscle insulin resistance during a hyperinsulinemic-euglycemic clamp (59), this is attributed to indirect effects of increased lipid accumulation via transcription and not a direct effect on insulin signaling or GLUT4 exocytic translocation proteins. The gene discussed is INS; the disease is Glucose intolerance.