Johnson et al. described two such mechanisms using a BRCA1 BRCA C-terminal domain-mutated breast cancer cell line: heat shock protein 90 (HSP90)-mediated stabilization of a mutant BRCA1 protein and mutations in the tumor protein p53 binding protein 1 (TP53BP1) that restore DNA end resection and facilitate RAD51 filament formation, key components of the HR repair pathway [44]. This evidence concerns the gene BRCA1 and breast carcinoma.