Investigations of NSCLC in various ethnic populations as well as cancers in gastrointestine, breast, and prostate have coordinately demonstrated that multiple Cns somatic mutations in KEAP1 cause dysfunction of the translated protein and in turn constitutive activation of NRF2, increasing risk of neoplasia and chemoresistance [12, 55, 58, 59]. This evidence concerns the gene NFE2L2 and neoplasm.