Indeed, the overexpression of the IR in cancer, first reported in breast tumors and related cell lines [97,98], has not been interpreted as relevant by the supporters of the “IGF1R mandatory-transducer” hypothesis, based on the assumption that the IR serves solely as a purely metabolic transducer, of which overexpression in cancer cells merely provides metabolic advantages over normal tissues with regards to nutrient consumption [12]. This evidence concerns the gene INSR and cancer.