Because oxidative stress responses interfere with a complex network of cellular mitochondrial detox enzymes, transcriptional regulators, and tumor suppressors—including NFκB, nuclear factor erythroid 2 like 2 (NRF2), and BRCA1—therapeutic strategies targeting with these processes with small-molecules or neutraceuticals and phytochemicals may hold promise for targeted tumor combination therapy and may reduce cytotoxicity of conventional therapies. This evidence concerns the gene NFKB1 and neoplasm.