Excessive adiposity‐induced insulin resistance and compensatory hyperinsulinemia have been shown to decrease hepatic synthesis of IGFBP‐1, which translates into increased concentrations of bioavailable IGF‐1, without modifications in serum total IGF‐1 levels (Lukanova et al., 2001; Maddux et al., 2006). The gene discussed is IGFBP1; the disease is Insulin resistance.