However, the present study found that forced expression of a mutant ARHGAP (Q158R) in Huh7 cells, which failed to inactivate Rac1 activity, had similar inhibitory effects on the proliferation, migration and invasion capacities of HCC cells without impairing Rac1 activity, as well as on the nuclear accumulation of β-catenin, a process regulated by Rac1 and considered to be crucial for β-catenin signaling activation. The gene discussed is RAC1; the disease is hepatocellular carcinoma.