IL1B and COVID-19: The different physiological conditions in T2DM patients modify the physiopathology of COVID-19, such as the immune dysfunction associated with impaired glycemic control and an increase in cytokine release associated with an attenuation of interferon response [5] and increased inflammation through SARS-CoV-2-infected monocytes that stimulate production of the pro-inflammatory cytokines IL-1β, IL-6, and TNF [6]; these changes were also recently described in patients treated with angiotensin-converting enzyme (ACE) inhibitors and angiotensin II type I receptor blockers (ARBs) [7].