Lastly, CKO-associated developmental defects were only suppressed by deletion of Brca1, not other tumour suppressor genes tested, including Trp53. This gene-specific genetic suppression most likely reflects a COBRA1-opposing action of BRCA1 in a specific functional pathway, rather than a more general, p53-like DNA damage checkpoint function in cell cycle arrest and/or apoptosis. This evidence concerns the gene NELFB and neoplasm.