In addition, our findings showed that treatment of cancer cells with specific JAK/STAT3 inhibitor AG490 blocked leptin-stimulated phosphorylation of both ERK1/2 and AKT, whereas pharmacological inhibition of either ERK1/2 or Akt pathway did not affect leptin-induced STAT3 phosphorylation (Fig 7A), suggesting that activation of JAK/STAT3 was upstream of the activation of the ERK1/2 and AKT pathways [35]. The gene discussed is AKT1; the disease is cancer.