Moreover, we confirmed that MAML1 could drive HCC tumour growth in vivo, which could be blocked by the inhibition of STAT3 signaling either by ruxolitinib administration or shRNA (Fig. 7F-I), suggesting that the tumour-promoting role of MAML1 is dependent on STAT3 signaling. The gene discussed is STAT3; the disease is hepatocellular carcinoma.