Their studies revealed that the expression of PTPRK was decreased in nasal-type natural killer T-cell lymphoma (NKTCL) human cell lines and primary tumors, and this decrease was inversely correlated with phosphorylated STAT3 (Y705) expression; the knockdown of PTPRK further decreased the expression levels of phosphorylated STAT3, whereas the overexpression of PTPRK reversed this effect, which resulted in increased NKTCL cell growth and invasion [61]. Here, STAT3 is linked to extranodal nasal NK/T cell lymphoma.