Noticeably, even though CD133 knockdown substantially decreased the expression of stemness-related genes be comparable to TIPRL knockdown in huh7 and SNU1097 cells, only TIPRL depletion significantly reduced cell viability and the self-renew ability of HCCs and iCCA (Figure 3B,E,F; Figures S8B,D,E and S9B,E,F), confirming our previous report that TIPRL works as an upstream for LC3 and CD133 [8], and thereby contributes to liver cancer cell proliferation, viability, and stemness, which are key events for liver cancer incidence/progression. This evidence concerns the gene PROM1 and liver cancer.