HLA-C and neoplasm: Considering that this recovery is mediated by MHC dependent recognition, that memory CD8+ T cells respond in the reduced activation threshold of tumor-specific cells, and that proliferated T cells have effector functions, administration of tumor specific antigens in the form of a vaccine or ex vivo expanded adoptive T cell transfer during this recovery period can induce disproportionate enhancement of effector cell populations that have autoimmune responses against tumor-associated self-antigens, leading to increased antitumor effect of ACT [180–184].