Oxidized LDL, which is increased in T2D, results in reduced proinsulin expression and JNK-mediated β-cell apoptosis, while HDL counteracts this adverse effect, possibly by inhibiting caspase-3 incision and activating AKT/PKB (Abderrahmani et al., 2007). The gene discussed is AKT1; the disease is type 2 diabetes mellitus.