This has also been linked to the reduction in the activity levels of transcription factors such as AP-1, C/EBP, and CREB.45 Finally, Hayakawa et al. investigated the role of ATF2 in determining the chemoresistance of breast cancer cells to DNA-damaging agents such as cisplatin, actinomycin D, methionine-S-methyl sulfonium chloride, and etoposide.46 The study suggests that JNK leads to a drug resistance phenotype by activating ATF2, which plays an important role in mediating augmented DNA repair through a p53-independent mechanism. This evidence concerns the gene ATF2 and breast cancer.