For example, SETDB1-dependent H3K9me3 represses the expression of T helper 1(Th1) cell-associated genes in CD4+ T cells by repressing a repertoire of ERVs that have been exapted into cis-regulatory modules to shape and control the Th1 gene network 5, which contributes to the generation of immune-permissive status in the tumor microenvironment. The gene discussed is CD4; the disease is neoplasm.