Although the molecular mechanisms that cause neoplastic transformation, and sustain tumour progression in the presence of INSR hyperexpression and/or hyperstimulation are not fully understood, an explanation for increased INSR expression in epithelial tumours has been recently provided by our group in both breast cancer cell lines and human breast cancer tissues, in which overexpression of the nuclear transcription factor activator protein 2-α (AP2-α) accounted for INSR overexpression [37] (Figure 2(a)). Here, INSR is linked to neoplasm.