Of interest, activation of the JAK-STAT pathway has also been implicated in CTCL progression, leading to constitutive expression of STAT3 and STAT5, upregulation of cell survival (Bcl-2 and Bcl-xL) and cell cycle genes (Cyclin D, c-Myc), Th2 cytokines (IL-4) and mir-155 [19]. The gene discussed is SOAT1; the disease is primary cutaneous T-cell non-Hodgkin lymphoma.