Additionally, Chen et al. showed that MALAT1 was involved in oxidative stress-mediated insulin resistance via the upregulation of the c-Jun N-terminal kinase (JNK), a stress-sensitive kinase, that upon activation, could suppress insulin signaling by inhibiting the phosphorylation of IRS and Akt, two major regulators of insulin-signaling cascades [109]. The gene discussed is AKT1; the disease is Insulin resistance.