Early in the COVID-19 pandemic Blanco-Melo et al. reported results from a transcriptome profiling study of various immortalized cell lines which demonstrated that SARS-CoV-2 infection elicited very low type I and III IFN and limited ISG responses, while inducing expression of pro-inflammatory cytokines genes19, raising the possibility that a deficient epithelial IFN response to SARS-CoV-2 may facilitate enhanced local viral replication that ultimately might lead to a dysregulated systemic pro-inflammatory response. Here, IFNA1 is linked to COVID-19.