An analysis of how the Type III CRISPR-Cas systems address viral infection, in conjunction with the presented mechanistic analysis of SisCsx1 ssRNA degradation, is strikingly reminiscent of the 2,5-oligoadenylate synthetase (OAS)/RNase L system, one of the principal IFN antiviral pathways29, which involves the activation of RNase L, an ubiquitous cellular endoribonuclease27. This evidence concerns the gene SMOC1 and viral infectious disease.