It may be argued, however, that, in these patients, T2D may either be a proxy of more advanced metabolic derangement which leads to excess fibrosis via NASH or that T2D per se exposes these individuals to higher risk of developing HCC via increased oxidative stress and hormonal changes (e.g., IR, increased IGF-1 and activation of the renin-angiotensin-aldosterone system) [193,212,213]. The gene discussed is IGF1; the disease is type 2 diabetes mellitus.