(A) Dipyridamole potentiates homeostatic adenosine receptor signaling by preventing reuptake of ectonucleoside (i) and by stabilizing the intracellular cAMP pools via inhibition of cytoplasmic phosphodiesterase (PDE) activity (ii). (B) Left unchecked, purinergic signaling exacerbates both inflammation and thrombosis; therefore, dipyridamole has the potential to inhibit multiple processes that have been recently linked to COVID-19 severity. Illustrated by Rachel Davidowitz.