In support, studies in animal models and cell-based assays following SARS-CoV-2 infection, as well as serum and transcriptional profiling of COVID-19 patients, revealed an exaggerated abnormal inflammatory response being marked by reduced levels of type I and III IFNs, along with increased chemokines and IL-6 expression in severe disease [38, 39]. The gene discussed is IL6; the disease is COVID-19.