COVID-19 risk-associated sequence variation at IFNAR2 may increase binding of ZNF410, a zinc finger protein involved in repression of fetal hemoglobin in erythroid cells [35], and risk variants also increase the predicted affinity of STAT3 for elements connected to IFNAR1, IFNAR2, PAXBP1, GART, C21ORF49, SON, and IL10RB. Variants connected to OAS1, OAS2, and OAS3 may affect the binding of 15 distinct transcription factors, including the RFX family of transcription factors involved in expression of MHC class II genes, and the plasmablast and TFH factors MIST1 (BHLHA15) [36] and ASCL2 [37]. This evidence concerns the gene IFNAR1 and COVID-19.