However, numerous factors could cause differences in efficacy between the two mAbs, including: the greater ability of anti-PD-L1 mAbs (IgG1) to induce antibody-dependent complement-mediated cytotoxicity [11]; the presence of a second ligand for PD-1, PD-L2, which cannot be blocked by anti-PD-L1 mAb [12]; and the potential for chemotherapy to modulate PD-L1 expression within the tumor microenvironment (TME) [13,14]. The gene discussed is CD274; the disease is neoplasm.