CD8A and neoplasm: In addition, it has been recently shown that while the increased mutational load would increase the formation of neoantigens whose exposure on the MHC-I complex elicit cytotoxic CD8+ and NK cells’ antitumor response, the intratumoral genetic variability (i.e., subpopulation of tumor cells with diverse mutation profile) would favor infiltration of macrophages (TAM), T regulatory cells (Treg), and myeloid-derived suppressor cells (MDSCs) which release pro-tumor factors, ultimately favoring a bad prognosis [77].