to be the first to demonstrate in the cytokine release syndrome (CRS) that the CDK7 covalent inhibitor THZ1 downregulates inflammatory gene transcription in macrophages after preferential target inhibition associated with SEs, such as STAT1 and IL1, decreases cytokine release, alleviates the hyperinflammatory state and rescues lethal CRS mice (191). The gene discussed is IL1B; the disease is congenital rubella syndrome.