The infection outcomes in the Axl-/-Mertk-/- mice were well explained by decreased IL-10 production from intralesional T cells as well as increased IFNγ and iNOS expression in T cells and myeloid cells, respectively, compared to WT mice, which phenocopys IL-10 deficient and anti-IL-10R antibody-treated mice, as previously reported [38]. The gene discussed is IFNG; the disease is infection.