Multiple genetic alternations have been identified in the progression of hepatocellular carcinoma (HCC),1 such as the inactive mutations of tumour suppressors (SWI/SNF complex, Axin and P53),2 and the active mutations of oncogenes (Kras, beta‐catenin and so on).3 These genetic alternations lead to the dysregulation of cellular pathways (such as Kras signalling, Wnt/beta‐catenin signalling, P53 signalling, SWI/SNF signalling).4 Fully understanding the activation of these signals would benefit the treatment. This evidence concerns the gene TP53 and hepatocellular carcinoma.