Furthermore, some studies have well described alterations affecting one to multiple cell fate-related nodes of the JAK/STAT pathway, including Hodgkin–Reed–Sternberg (HRS)-like “cells of NK phenotype” [29], primary cutaneous γδ T cell lymphoma (PCGDTL) [30], EITL [31], post-transplant lymphoproliferative disorder (LPD) [32] and CTCL [32], part of which led to upregulated JAK phosphorylation and activation. The gene discussed is SOAT1; the disease is primary cutaneous T-cell non-Hodgkin lymphoma.