According to the longstanding “clonal evolution” model of carcinogenesis, cervical carcinoma has long been described as a consequence of unlimited and uncontrolled cellular proliferation conferred by multiple genetic and/or epigenetic mutations that can hit any somatic cells within the tissue. However, in the last few years, accumulating evidence has suggested that the capacity of initiating a tumor, including cervical carcinoma, is rather a unique feature of a small subset of stemlike cells called “cancer stem cells” (CSCs) or “tumor-initiating cells.” CSCs have the exclusive ability to self-renew expanding the CSCs pool, and to maintain the tumor differentiating into the heterogeneous non tumorigenic cancer cell types which constitute the majority within the tumor.1 Although solid evidence is lacking to date, subcolumnar reserve cells emerged to be the best candidate for cervical stem cells, which provide a depository for the regeneration of the mucous-forming epithelium. S