These controversial results may be explained by several reasons including (i) exonucleases other than XRN1 can contribute to sfRNA formation, (ii) depletion of XRN1 causes changes in total cellular RNA level that may include products of endonucleolytic cleavage, and (iii) reduction in XRN1 may contribute to differences in susceptibility to viral infection [7]. The gene discussed is XRN1; the disease is viral infectious disease.