The direct basis for this work stems from the observation that CpGs linked to silencing of the well-known BRCA1 tumor suppressor gene display a two-population CpG methylation pattern in triple negative breast cancer (TNBC, tumors that are negative for estrogen and progesterone receptor expression and lack amplification of the human epidermal receptor growth factor 2/erythroblastic oncogene B, HER2/ERBB2, gene) highly correlated with tumor cell content estimated from whole genome sequencing [24]. The gene discussed is BRCA1; the disease is triple-negative breast carcinoma.