TMEJ protects from replication stress by preserving genomic integrity at the cost of mutations in most breast cancer subtypes, except in BRCA non-mutated claudin-low subtypes, in which the important contribution of ZEB1 as a protective actor in both early and late steps of tumor development has been demonstrated (Morel et al., 2017; Pommier et al., 2020; Prodhomme et al., 2021). This evidence concerns the gene ZEB1 and breast carcinoma.