Our analysis suggests that changes in the systemic flux of mitochondrial TCA cycle intermediates may stem from metabolic pathway dysregulation in COVID-19 patients, potentially related to mammalian target of rapamycin/hypoxia-inducible factor-1 signalling and glycolytic regulation caused by mitochondrial dysfunction [37], making it a candidate for dysregulation by COVID-19 [38]. The gene discussed is MTOR; the disease is COVID-19.