Taken together, we suggest that NDRG1 could be involved in the EMT/CSCs dynamics, where a sustained exposure to TGFβ1 on tumor cells in the primary tumor site would induce the initial activation of EMT and further maintenance of different CSC phenotypes to promote distant invasiveness and chemoresistance through the generation and maintenance of mixed populations of tumor-initiating cells, including those with slow cycling features (ALDH1+, CD44+/CD24- and side population). The gene discussed is CD24; the disease is neoplasm.