CHEK2 functions downstream of ATM (Ataxia-telangiectasia mutated) to phosphorylate several substrates, including TP53 (Tumour protein p53), Cdc25C (Cell division cycle 25C) and BRCA1 (Breast cancer 1, early onset), leading to cell cycle arrest, activation of DNA repair or apoptosis in response to DNA double-stranded breaks. This evidence concerns the gene BRCA1 and breast carcinoma.