Whole genome sequencing analyses from a Swedish database revealed that among TNBC carriers harboring a high HRDetect mutational signature, 67% was explained by germline/somatic BRCA1/2, as well as by other genomic/epigenic abnormalities (BRCA1 promoter hypermethylation, RAD 51C hypermethylation, or biallelic loss of PALB 2), illustrating the existence of many alternative alterations that may lead to HRD tumor status [42]. The gene discussed is BRCA1; the disease is neoplasm.