Integration of the HBx sequence into host DNA in HCC promotes genetic instability through mechanisms that include the inactivation of the UV-damage DNA binding protein, so as to interfere with nucleotide excision repair, repression of p53-mediated gene transcription [155] and inactivation of p53-dependent apoptosis, cell cycle regulation, DNA repair and tumor suppression [156]. Here, TP53 is linked to neoplasm.