Loss of BRCA1/p220 tumor suppression function often leads to profound increase in genomic instability [5,6], likely due to lack in DNA damage repair [7], in cell-cycle checkpoints activation [8] or in ubiquitylation-mediated degradation of proliferation (e.g., estrogen receptor [ER]) or survival (e.g., AKT) proteins [9-11]. Here, BRCA1 is linked to neoplasm.