Modelling the regulome of host genesinduced by COVID-19 and the drugs that could normalize these genes both implicated theJAK1/2-STAT1 signaling system downstream of type I interferon receptors, and NF-κB.Ruxolitinib, a JAK1/2 inhibitor and the top predicted pharmaceutical candidate, normalizedinterferon signature genes, IL-6 (the best characterized severity marker in COVID-19) andall complement genes induced by SARS-CoV2, but did not affect NF-κB-regulatedgenes. The gene discussed is IL6; the disease is COVID-19.