Furthermore, we now have evidence that mutations in TP53 and EGFR attenuate ROS accumulation in cancer cells by sustaining an oncogenic oxidant intracellular environment through an integrated regulation of redox-related enzymes and signaling pathways (e.g. PI3K-AKT signaling, MAPK cascade, ERK and the redox-sensitive IκK/NF-κB pathway)113,114, thereby supporting proliferation, protein synthesis and invasion106,115–118. The gene discussed is EGFR; the disease is cancer.