In a recent biomarker driven study of the Jak1/2 inhibitor ruxolitinib in patients with PTCL (n = 45) and MF (n = 7) [82], patients were stratified into three different groups based on their dysregulation of the Jak/Stat pathway: (1) activating Jak/Stat mutations, (2) pStat3 overexpression, or (3) no mutations or overexpression. This evidence concerns the gene SOAT1 and mature T-cell and NK-cell non-Hodgkin lymphoma.