HIF1A and triple-negative breast carcinoma: Hypoxia induction of the UPR, resulting alternative unconventional XBP1s splicing, promotes XBP1s complexing with HIF-1α, influencing HIF-1 transcriptional function by recruiting RNA polymerase to the promoters of pro-angiogenic VEGFA, metabolic PDK1 and GLUT1 regulators, and DDIT4 negative mTOR regulators, increasing their expression in triple-negative breast cancer (TNBC) [150].