The reasons for NRF2 activation in tumor tissue can be mutations in KEAP-1 [47] causing Keap-1 not to be able to bind to NRF2, resulting in constitutive NRF2 activation, increased ROS formation because of increased metabolism of fatty acids [5], and increased influx of unfolded proteins into the endoplasmatic reticulum (ER) inducing ER-stress [48]. The gene discussed is KEAP1; the disease is neoplasm.