In this regard, taking into consideration that PCSK9, which is found to be enhanced by hypoxia/reoxygenation (Yang et al., 2020), has also shown to degrade CD36 beyond the LDL-R (Demers et al., 2015), PCSK9 inhibition might hold promise as a therapeutic strategy to modulate myocardial CD36 content and expression and consequently FA metabolism levels in the setting of MI. The gene discussed is PCSK9; the disease is myocardial infarction.