HNF1B and Miyoshi myopathy: These observations might be explained, at least in part, by the stimulatory effects of T2D-associated hyperglycaemia, insulin resistance and resulting hyperinsulinemia on MM cell growth [26, 27] but also by the deregulation of tumour-suppressor genes linked to T2D (such as CDKN2A-2B, KCNQ1, HNF1B) [28–30] that might lead to uncontrolled cell proliferation, cell differentiation and disease progression and, consequently, to shorter survival periods.