Under both control and maximal insulin treatment, glucose uptake and GLUT4 translocation were increased in C2C12 myocytes overexpressing FAK, implying that increased FAK protected C2FAKwt/+ (FAK overexpressing) cells from hyperinsulinaemia‐induced insulin resistance, whereas C2FAKmut/+ (FAK tyrosine‐397 mutated) cells developed insulin resistance. The gene discussed is SLC2A4; the disease is Insulin resistance.