Our data, showing faster dephosphorylation of both pChek1 and pP53 in AEP-deficient cells, suggest that reduced phosphatase activity in BC cells could account for the prolonged activation of Chek1 and P53 shown in control MDA-MB-231 cells compared with AEP KD cells (Fig. 4C), with previous works suggesting a potential role for AEP as a regulator of protein phosphatase activity [56–58]. This evidence concerns the gene LGMN and breast cancer.