Enteroviral infection is known to limit expression of ISGs via multiple mechanisms including degradation of IFNAR1 [31] as well as blocking JAK-STAT signaling downstream from the receptors by induction of KPNA1 degradation [32], YTHDF3 cleavage [33], and induction of SOCS1 and SOCS3 expression (negative regulators of JAK-STAT signaling) upon infection [34]. This evidence concerns the gene SOCS1 and enterovirus infectious disease.