SOAT1 and primary cutaneous T-cell non-Hodgkin lymphoma: Interestingly, loss of regulatory control through deletion, epigenetic silencing, or functional deviation of Jak/STAT signaling inhibitors such as SOCS1, SOCS3, SHP-1, and HNRNPK also appears to be implicated in aberrant cytokine signaling [26–30] indicating that a dynamic, multifactorial interplay between genetic, epigenetic and environmental triggers drive disease progression in SS and other variants of CTCL.