INS and neoplasm: The possible pathogenetic mechanisms implied seem to be different for each neoplasm8: both altered adipocyte function and insulin resistance determine an increase in circulating levels of hormones, such as oestrogens, insulin and insulin‐like growth factors, which may in turn enhance tumour proliferation and inhibit apoptosis8; furthermore, adipokines may contribute to oncogenesis by stimulating chronic inflammatory mediators, increasing oxidative stress and impairing immune responses.9