The strong correlations between several baseline signature scores and the residual Ki67 confirmed the high proliferation (AURKA-GS, PTEN-GS, Gene70-GS, GGI-GS, CIN70-GS), RB-loss (Rbloss-GS, DiLeoRBloss-GS), high E2F activation (E2F4activation-GS, E2Factivation-GS), and TP53 dysfunction (TP53-GS) were associated with high-oestrogen independent residual proliferation irrespective of whether the tumour showed an antiproliferative response to AI [12, 17–21]. This evidence concerns the gene TP53 and neoplasm.