Interestingly, while investigating a mutation within the ATP binding motif, it was found that the ectopic expression of a SNRNP200 C502A variant elicited an IFNB1 response independent of viral infection (S11 Fig) in line with the recently reported natural gain-of-function of DDX58 and IFIH1 ATPase-deficient variants [29]. This evidence concerns the gene IFIH1 and viral infectious disease.