The WB analysis showed that C1orf122 knockdown induced a sharp rise in Bax protein levels, phosphorylated Bcl-2 levels, Cleaved-Caspase-3 levels, and downregulation of total Bcl-2 protein and total Caspase-3 levels, further confirming that C1orf122 knockdown significantly promoted HCC cell apoptosis (Fig. 3C; Fig. S6E and S6F). The gene discussed is BCL2; the disease is hepatocellular carcinoma.