During the oncogenesis of pancreatic cancer, YAP mediated epithelial‐mesenchymal transition (EMT) and cancer cell proliferation.40 Additionally, MST1/2 deficiency resulted in cell overgrowth and hepatocellular carcinoma (HCC), and overexpression of MST1 and MST2 could suppress HCC development through inactivation of the YAP oncogene.41 The absence of Sav1 or MST1/2 may lead to bigger liver, causing the formation of tumors.42 In present study, we found that MST1 was down‐regulated while YAP was up‐regulated in NKTCL tissues and cells. This evidence concerns the gene STK3 and hepatocellular carcinoma.