Until 1999, three IFN-responsive antiviral proteins had been considered to be involved in the antiviral processes: the Mx (for myxovirus resistance) dynamins, the double-stranded RNA-dependent protein kinase (PKR) and the 2′-5′ oligoadenylate synthetases that function through RNase L. The demonstration that IFN confers resistance to viral infection in cells derived from mice triply deficient (TD) in PKR, Mx1 and RNase L [33] revealed the implication of other antiviral pathways. The gene discussed is RNASEL; the disease is viral infectious disease.