For the severe COVID-19 cases, except the ~19% with life-threatening pneumonia that is caused by IFN-deficiency functionally through genetic and autoimmune errors as described above [31,39], the severity progression in the other majority of severe COVID-19 patients may be underlain by epigenetic regulation of host factors connected to the IFN and chemokine signaling pathways as genetically elucidated [22,23,24]. This evidence concerns the gene IFNA1 and hyperinsulinemic hypoglycemia, familial, 4.