In contrast to IFNγ, the role of FasL:Fas interactions in the LCMV model appears more limited—both FasL- and Fas-mutant mice (FasLgld and Faslpr strains, respectively) control an acute LCMV infection [31]—yet a non-redundant role for Fas in virus clearance or CD8+TM generation could be readily demonstrated in mice with compound immunodeficiencies [32–34]. Here, FASLG is linked to Immunodeficiency.