One proposed mechanism for the improvement of endothelial function following Nrf2 activation is the increased expression of a subunit of the BK (big potassium or large conductance, Ca2+-activated potassium) channel, the BK-β1, and its attenuated degradation (Lu et al., 2017), a process commonly accelerated by diabetes-induced oxidative stress (Li et al., 2017). This evidence concerns the gene NFE2L2 and diabetes mellitus.