During the eosinophil-dependent protective response in primary in vivo infection with either B. malayi Mf or S. stercoralis L3, EPO is released into the bloodstream [5], [9] and deficiency of EPO or MBP-1 can enhance the establishment of L. sigmodontis L3 in non-permissive mouse strains [14]. The gene discussed is EPO; the disease is infection.