In HPV infection, viral helicase, E1, promotes UAF1-USP1 activity for viral genome replication [66,67] and the high-risk HPV oncogenes, E6 and E7, delay UAF1-USP1 mediated deubiquitination of the Fanconi anemia (FA) DNA crosslink repair, contributing to genomic instability [68]. Here, USP1 is linked to Friedreich ataxia.