This mechanism has been demonstrated by McCormack and colleagues in a series of mouse studies [90] and subsequently expanded to humans by Vonderheid and colleagues [91] in a cohort of 49 CTCL patients in which a majority of whom exhibited increased Vβ5 usage relative to other Vβ families, usually predominant in normal CD4 T cells. The gene discussed is CD4; the disease is primary cutaneous T-cell non-Hodgkin lymphoma.