The fact that COVID-19-associated inflammation itself predisposes to cardiac arrhythmia and inhibits the activity of CYP3A4, potentiates the risk of drug induced-QTc prolongation even more as evidenced by the increased reporting of QTc prolongation during the COVID-19 pandemic, particularly among male patients19. The gene discussed is CYP3A4; the disease is chronic obstructive pulmonary disease.