Their oncoproteins, namely E6 and E7, from these high-risk genotypes have been shown to modulate several key signalling pathways, including inactivation of p53, induction of hTERT, binding to PDZ by E6 and inactivation of pRb and related pocket proteins, activation of E2Fs by E7, which leads to inhibition of DNA-damage response, inhibition of apoptosis, inhibition of differentiation, induction of genomic instability, and deregulation of the immune response and cellular energetics and thus fosters immortalization, transformation and tumour progression [6,60]. Here, TP53 is linked to neoplasm.