This is supported by the findings that E6-binding competent pep11 variants (i) have a much higher in vitro binding affinity for HPV16 E6 than the E6AP interaction domain [16,19], (ii) can restore intracellular p53 protein levels in HPV16-positive cancer cells that endogenously express E6AP [16,19], and (iii) can compete for HPV16 E6 / E6AP binding. Here, UBE3A is linked to cancer.