However, in cancer cells, overactivation of NFE2L2 - often due to mutations in KEAP1 or gain-of-function mutations in NFE2L2 - leads to enhanced tumor survival by promoting antioxidant defenses, metabolic reprogramming, and resistance to oxidative stress-induced cell death, such as ferroptosis and apoptosis[6]. Here, KEAP1 is linked to neoplasm.