MAML1 and papilloma: It was shown that an E6 MAML binding mutant could not inhibit Notch signaling and that this mutant was unable to form papillomas in vivo. As such, it was postulated that this pathway may be involved in the phenotype observed in the high-density competition assay, and that similar interference with MmuPV1 E6 MAML1 binding in this model could indicate whether the downstream Notch signaling pathway was involved in modulation of the persistence phenotype.