As JAK3-activating mutation was frequent in NKTCL pathogenesis, the pan-JAK inhibitor Tofacitinib efficiently reduced phosphorylated STAT5 and cell viability in JAK3-mutant and wild-type NKTCL cell lines and mouse xenografts [19,24]. This evidence concerns the gene JAK3 and extranodal nasal NK/T cell lymphoma.