Thus, GEP-B tumors had: i) enhanced self-defense mechanisms against complement-dependent cytotoxicity, as reflected by overexpression of the KIT mast cell-associated molecule [51]; ii) defective expression of major histocompatibility complex (MHC) molecules which are that frequently involved in tumor immune escape [52], and/or; iii) greater cancer-driven immunosuppression as a consequence of increased expression of the programmed cell death 1 ligand 2 (PDCD1LG2) [53] and the VGFC [51] genes. The gene discussed is PDCD1LG2; the disease is cancer.