At the genomic level, TNBC are characterized by early structural aberrations that persist through clonal evolution and by a high incidence of TP53 mutations [5–9]; TNBC mutation load is more than ten times higher as compared to luminal carcinomas [9] but, with the exception of TP53, mutations and mutated genes are non-recurrent among tumors and may be heterogeneously affected within the same tumor [6, 9]. Here, TP53 is linked to neoplasm.