From a gene-specific point of view, Nindrea et al. showed that hypermethylation at the BRCA1 promoter can act as “hit” by down-regulating transcription and initiating loss-of-function, thus disrupting the DNA damage repair response [49,50], which serves as an excellent biomarker for elevated risk of hereditary triple-negative breast cancer (TNBC) cases [51]. This evidence concerns the gene BRCA1 and triple-negative breast carcinoma.