Recent studies have shown that the HIF-1 pathway is overactive in TNBC, compared to other isotypes, and that the HIF-1 protein is overexposed in more than 80% of TNBC patients.[13,14] Several signaling pathways, noncoding RNA, inflammatory mediators secreted by tumor cells, in the TNBC tumor microenvironment of oxygen levels, and other factors could all play a role. Here, HIF1A is linked to neoplasm.