IL1B and COVID-19: Conditioned media obtained from metabolically primed SARS-CoV-2 infected monocytes compromise CD4 or CD8 T-cell proliferation and also induce lung epithelial cell death.1 Inhibition of HIF-1α, as well as neutralization of ROS or IL-1β antagonize such effects and restore T-cell function or lung epithelial cell survival, which suggests that increased glucose metabolism through aerobic glycolysis and subsequent cytokine production in monocytes could further deteriorate neighboring cells in a paracrine fashion under pro-diabetic conditions in COVID-19 patients (Fig. 1).