also confirmed showed that HSV-TK/GCV therapy is at least partially dependent on p53 status in tumor cells evident as the expression of exogenous p53 and the overexpression of ASPP2 that interacts with endogenous p53 can enhance HSV-TK/GCV-induced cell death in HCC cells lacking functional p53 (Liu et al., 2016). The gene discussed is TP53; the disease is neoplasm.