With this regard, the infection has been reported to attenuate the expression or activation of significant factors related to DSBs repair, including Meiotic Recombination 11 Homolog A (MRE11), Nijmegen Breakage Syndrome 1 (NBS1), Ataxia Telangiectasia and Rad3-Related Protein (ATR), ATR-Interacting Protein (ATRIP), RAD51 and RAD54L with a more prominent modulation of DDR observed in the infection with cagPAI-positive compared to cagPAI-negative strains [27,30]. This evidence concerns the gene RAD54L and infection.