The protective effects of NRF2 activation against pathophysiological apoptosis have been reported using several types of disease models, such as osteoarthritis, ischemia-reperfusion, and diabetic skin ulcers (Khan et al, 2018; Long et al, 2016; Meng et al, 2017), where neutralizing excess ROS levels by NRF2 mediated redox regulation seems to be one of the potential mechanisms. This evidence concerns the gene NFE2L2 and osteoarthritis.