While several subtypes thrive in severe immune suppression (EBV-related DLBCL in general), cHL is dependent on an at least partially functioning immune system due to HRS cell interaction with the microenvironment, particularly their dependence on CD4+ T-cell signaling (122), and thus their restoration by HAART “paradoxically” promotes cHL development. The gene discussed is CD4; the disease is classic Hodgkin lymphoma.