Delays in IFN production58, intrinsic defects in pattern recognition or IFN signalling59–62, low expression of IFNAR221,63 or the production of anti-IFN autoantibodies57,64,65, all associated with severe COVID-19, may facilitate the initial infection of monocytes/macrophages in a manner similar to the effects of ruxolitinib, leading to positive feedback loops and detrimental levels of inflammation11. Here, IFNA1 is linked to infection.