There has been a theoretical uncertainty in regard to the safety of ACEI/ARB use in patients with COVID-19 based on the ACE2 viral entry mechanism [71, 72]. The virus gains cellular entry by attaching to the ACE2 receptor [72]. ACE2 expression and activity have shown to be increased in by ACEI/ARB use [73]. Although there is theoretical risk that ACE2 upregulation may increase the susceptibility of infection, other conflicting evidence indicates that upregulation of ACE2 in fact has a more protective effect. Studies in mouse models have shown that ACE2 is protective against acute lung injury and blocking the renin-angiotensin-aldosterone system pathway decreases lung failure [74, 75]. Based on the review of the literature to date, the Heart Failure Society of America recommends continuation of ACEI/ARB use for patients that are prescribed them for heart failure, hypertension, and ischemic disease [76••]. Abrupt discontinuation of medications is not recommended and can worsen clinical stability especially in patients with existing cardiovascular conditions [71].