As some human cancer types, including HCC, exhibit an abnormal p53 gene or have disrupted p53 gene activation pathways, the effect of GRA16 should be evaluated in conditions with and without the p53 gene.17 Thus, in our study, we developed genetically modified GRA16‐stable cancer cells for p53‐wild‐type HepG2 and p53‐null‐type Hep3B, and examined the binding between GRA16 and HAUSP within cells using the co‐IP. This evidence concerns the gene USP7 and hepatocellular carcinoma.