Recent studies prove that mechanisms and treatment susceptibility of BRCA-mutant tumors are not restricted to inherited tumor – both familial and sporadic tumor share common clinical features [5]: extreme levels of genomic instability, basal-like transcriptomic signature (genes expression profile similar to normal breast myoepithelial layer), and triple-negative phenotype (oestrogen receptor, progesterone receptor and ERBB2 oncogene not expressed or amplified). Here, PGR is linked to neoplasm.