KDM7A and neoplasm: In this subtype tumor biology and clinical contexts, the pro-oncogenic role (poor prognosis) at higher expression KDMA7-DT within BLBC patients can be explained directly due to high enrichment of the gain and amplification event in triple-negative/basal type primary tumors and indirectly by TP53 missense mutations downregulating at transcriptional level TP53 mRNA levels, that (as we showed in semi-transformed fibroblasts model) can inhibit KDM7A-DT’s stress-induction levels.