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A specific oxidoreductase, previously known as apoptosis-inducing-factor mitochondrial-2 (AIFM2), capable of recycling reduced ubiquinol (Co-enzymeQ 10 H 2 ) from ubiquinone at the expense of NAD(P)H, has been presented as a potential ferroptosis inhibitor due to the fact that its overexpression complements the loss of GPx4 in PFA1 and human fibrosarcoma (Figure 2)

The health benefits of significant weight loss typically outweigh the temporary or manageable inconvenience of addressing this side effect