In conclusion, our data suggest that, in BC cells, AEP contributes to genotoxic tolerance by reducing DNA damage signaling through a reduction in ATR levels, while promoting sustained pChek1 and pP53 phosphorylation to arrest the cell cycle and promote DNA repair through the regulation of PPP1R10 levels and PTW/PP1 complex, thereby allowing cancer cells to scape DNA damage-induced cell death [62, 63]. The gene discussed is ATR; the disease is cancer.