To overcome the prenatal lethality of Socs1 deficiency during development (13, 15, 16) and frame the Socs1 deletion in CD4 T cells specifically, thus enabling studies on the contribution of Socs1 in the pathogenesis of mycosis fungoides, we used cross breeding of two existing transgenic mouse strains (Socs1flox and Cd4Cre). This evidence concerns the gene CD4 and mycosis fungoides.