In summary, we conclude that the high expression of FAM21C in HCC tissues can promote the malignant progression of HCC, and its mechanism involves the inhibition of CAPZA1 capping function by FAM21C which binds to CAPZA1, leaving the F-actin barbed-end in an open state, which in turn induces the remodeling of the F-actin cytoskeleton, thus promoting the invasion and migration of HCC cells. This evidence concerns the gene CAPZA1 and hepatocellular carcinoma.