Further analysis suggests that impairment of Th17-to-FoxP3+ T cells along with induction of FoxP3+−to-Th17 (58)-to-Th1-like (61) IFN-γ producing cells transdifferentiation can be a reliable approach for Treg cells depletion within the tumor microenvironment, due to the inability of committed Th1 to convert to Treg in Th1-Th17-Treg axis (55). The gene discussed is FOXP3; the disease is neoplasm.