We hypothesize (Figure 1) that, at early stages of tumor development γδ T cells of the γδ1 type producing cytokines with proven anti-tumor activity (IFN-γ and TNF-α) and equipped with cytotoxic potential either expand locally (Vδ1) or are recruited at the tumor site from peripheral blood (Vδ2) and may exert anti-tumor activity; however, with tumor progression, factors produced in the microenvironment cause polarization of γδ cells from γδ1 to γδ17 and γδreg, which instead promote tumor progression. The gene discussed is IFNG; the disease is neoplasm.