To investigate the mechanism underlying the upregulation of p-FAK in HCC cells following sorafenib treatment, we focused on the canonical RhoA/ROCK axis, which is widely implicated in FAK activation (26, 27, 28); Notably, RhoE competitively binds to ROCK in place of RhoA, and the interaction between RhoE and ROCK inhibits ROCK activation. The gene discussed is RHOA; the disease is hepatocellular carcinoma.