We hypothesized that PIM kinase inhibition could be of therapeutic value in PTCL because: 1) PIM kinases have an important role in CD4+ T cell responses [28]; 2) PIM1 and especially PIM2 expression is increased in PTCL patients, cell lines and primary tumoral T cells of Sézary Syndrome patients; 3) they are significantly correlated with survival pathways, such as Jak/STAT, NF-κB and IL-2 signaling; and 4) pharmacological PIM inhibition is effective in other T cell-mediated malignancies, such as T cell acute lymphoblastic lymphoma [29]. Here, SOAT1 is linked to mature T-cell and NK-cell non-Hodgkin lymphoma.