ENO1 and neoplasm: Several mechanisms were demonstrated to be responsible for this effect: the induction of anti-ENO1 antibodies, which mediated complement-dependent cytotoxicity, inhibited tumor cell invasion [18,19] and myeloid-derived suppressor cell (MDSC) infiltration into the tumor [20]; and the expansion of Th1 and Th17 cells, which contributed—with their cytokine—to inhibit tumor cell growth and to elicit the B cell-isotype switch.