We have previously demonstrated that signaling via IL-4Rα plays the major role in the non-healing response of BALB/c mice following infection with L. mexicana[6] and that IL-4Rα−/− mice, unlike their wild-type counterparts that produce progressively growing non-healing lesions, display a non-lesion growth disease phenotype associated with an enhanced type-1 response. This evidence concerns the gene SGCG and infection.