Downregulation of the insulin receptor can inhibit cancer cell proliferation and metastasis, altering downstream signalling in vivo.48 It has been shown that insulin receptors have a high affinity for insulin (±10−10 mol/L), while IGF1R has a higher affinity for IGF1 and IGF2 (±10−10 mol/L), which is 100‐fold higher than that for insulin.49 Our data suggest that the KRAS mutation, rather than insulin, can induce an increased expression of insulin receptors, the mechanism of which warrants further study. This evidence concerns the gene INSR and cancer.