Our western blot results subsequently indicated that the activity of CHK1 pathway was slightly elevated in Mus81‐inhibited HepG2 cells after CHK2 inhibition, thereby promoting the activity of p53, Bax, and Caspase‐3, which might be the mechanisms underlying the deteriorative S‐phase arrest and apoptosis induced by CHK2 inhibition in Mus81 depleted HCC cells. Here, BAX is linked to hepatocellular carcinoma.