Previous studies have shown that NLRC5 was up-regulated in tumor tissues of HCC patients, and in vivo studies in mice have found that NLRC5 knock-down inhibited tumor growth by blocking the Wnt/β-catenin signaling pathway.26 Besides, NLRC5 can also regulate the expression of VEGF-A through the activation of the PI3K/AKT signaling pathway to mediate tumor angiogenesis and proliferation.27 At the same time, we also verified through the database that NLRC5 is associated with critical factors (such as CTNNB1 and VEGFA) related to the activity of these pathways (Figure S2). This evidence concerns the gene AKT1 and neoplasm.