Insulin is a potent regulator of hepatic SHBG output, which is suppressed in the context of hyperinsulinaemia, leading to reduced SHBG, and therefore increased free androgens, in insulin‐resistant states such as PCOS in women.40 It is unlikely, however, that SHBG independently plays a causal role in the pathophysiology of metabolic diseases such as T2DM. The gene discussed is SHBG; the disease is type 2 diabetes mellitus.