The mechanisms responsible for this are: recreation of BRCA1/2 activity, observed in clinical trials in patients with BRCA1/2m cancers (Kondrashova et al., 2017) (reverse mutations (Domchek, 2017) or gene fusion under the transcriptional control of heterologous promoter (Ter Brugge et al., 2016)) and suppression of NHEJ (caused by specific 53BP1 mutation in BRCA1 protein sequence) (Bouwman et al., 2010) (Hurley et al., 2019). Here, BRCA1 is linked to cancer.