Mechanistic studies using cell culture systems have provided empirical proof that infection with C. trachomatis induces DNA double-strand breaks (DSBs) in cells while impairing the repair process by inhibiting recruitment of ataxia telangiectasia mutated kinases (ATM) and p53-binding protein 1 (53BP1), further to inducing production of the epidermal growth factor (EGF), which is implicated in dysplasia (Chumduri et al., 2013; Patel et al., 2014). Here, TP53BP1 is linked to infection.