Since we observed that HLJ1 expression was negatively correlated with SOCS3 but not with IL-6, LIF, ROS, or EGFR, further analysis of JAK1/2 activation could offer deeper insights into the molecular mechanisms by which HLJ1 regulates peritumoral STAT3 activation and subsequent liver cancer niche formation. The gene discussed is DNAJB4; the disease is liver cancer.