These data postulated the hypothesis that cutaneous bacteria, such as B. safensis, which drive the clonal proliferation of skin-homing, cutaneous lymphocyte-associated antigen (CLA)+, chemokine (C-C Motif) receptor 4 (CCR4+) CD4+ T cells, may also induce the activation of malignant T cells and tumorigenesis in patients with CTCL [68]. The gene discussed is SELPLG; the disease is primary cutaneous T-cell non-Hodgkin lymphoma.