The identification of this quiescent pathogen-specific CD4+ T-cell subpopulation, which was resistant to chemotherapy-induced cytotoxicity and subsequently expanded in AML patients, formerly rendered lymphopenic by chemotherapy, therefore contributing to repopulation and maintenance of anti-viral immunity, may spur further investigations on similar mechanisms that could preserve and sustain the emergence of endogenous long-lasting anti-leukemic specific immunity [46,47]. This evidence concerns the gene CD4 and acute myeloid leukemia.