CD4 and T-cell large granular lymphocyte leukemia: The most accepted hypothesis is a clonal drift of a T cell population after chronic antigen exposure, as suggested by cross-reactivity to human T-cell lymphotropic virus 1 (HTLV-1) epitopes or a frequent concomitant chronic viral infection in LGL leukemia patients, especially EBV, hepatitis C virus (HCV), or cytomegalovirus (CMV), especially in CD4+ T-LGL [1,26,27,28,29].