HIF1A and neoplasm: The majority of TNBC have activated RAS-RAF-MEK-ERK, which prolongs tumor cell viability by regulating downstream caspase-mediated apoptosis pathways and is correlated with TNBC chemo-resistance and progression.[42] ROS can activate ERK, because low concentrations of ROS can promote the activation of ERK through the classic Ras-Raf-MEK pathway, thereby promoting the transcriptional activation of HIF-1α.