We hypothesize that immune checkpoint mediated PTCL proliferation is amenable to targeting by inhibiting AK and PI3K and that these targets can be developed as a novel therapeutic strategy.Immunohistochemistry (IHC) of tumor samples from patients treated with alisertib for relapsed and refractory PTCL (SWOG 1108) [6] showed high Ki-67 and a PD-L1:PD-1 staining ratio of 8.9 fold. This evidence concerns the gene CD274 and mature T-cell and NK-cell non-Hodgkin lymphoma.