This mechanism appears to involve the reprogramming of quiescent EpCAM+/ABCG2+ CSCs to the TSD phenotype, characterized by transient expansion (rapid proliferation under hypoxic conditions), cytoprotective factor secretion (secretion of factors like glutathione (GSH), potentially protecting neighboring tumor cells from cisplatin-induced toxicity), and altruistic apoptosis (a transient state that undergoes spontaneous apoptosis in vitro and disappears during serial transplantation in vivo, suggesting a potential self-sacrificing mechanism for the benefit of the tumor self-identity). This evidence concerns the gene ABCG2 and neoplasm.