NFE2L2 and neoplasm: The results collectively found that in kallikrein-related peptidases (KLK) tumor cells, activation of the KEAP1/NRF2 pathway limits metabolic flexibility and promotes glutamine-addictive metabolism to maintain the tricarboxylic acid (TCA) cycle in addition to redox homeostasis, rendering these tumor cells selectively vulnerable to glutaminase inhibitors (143).