By generating NAD(P)H quinone oxidoreductase 1 (NQO1) knockout (NQO1−/−) cells from the HCEnC-21T line, effectively removing the enzyme that breaks down MN, and comparing the effects of MN on both regular and NQO1-deficient HEnC-21T, it was found that the absence of NQO1 amplified the severity of MN-induced EndMT, suggesting a protective role against oxidative stress and potentially driving FECD progression [44]. Here, NQO1 is linked to Fuchs endothelial corneal dystrophy.