SOAT1 and primary cutaneous T-cell non-Hodgkin lymphoma: However, abnormalities in cytokine production [6-10], a cytokine-independent constitutive activation of the Janus kinases (JAKs)/Signal transducer and activator of transcription (STAT) pathway [11-13] and aberrant regulation of nuclear factor κB (NFκB) [14-17] are known to play a key role in the pathogenesis of CTCL.