Consequentially, the explanation for the large compensative expansion of monophenotypic CD45RA−CCR7− CD4 T cell responses in ASCT recipients could be a high antigenic exposure to self peptide, including tumor antigens [29], or, alternatively, to nonself peptides, such as normal flora in the gastrointestinal [GI] tract–gut commensals, that have been recognized as the dominant force for rapid proliferation of T cells in severely immunodeficient host [28]. The gene discussed is CD4; the disease is neoplasm.