This phenomenon, termed “senescence-associated stemness”,150 is further exemplified in liver cancer, where non-stem (EpCAM-/CD133-) cells transition into Wnt/β-catenin-activated CSCs post-senescence, enhancing tumor initiation.66 Another study151 showed that some senescent breast cancer cells are able to escape senescence and establish stable colonies with a CSC-like aggressive phenotype characterized by elevated CD133 and Oct4 expression. This evidence concerns the gene PROM1 and breast carcinoma.