In particular, we recently demonstrated that poor cardiac lymphangiogenesis post-MI was linked to elevated interferon (IFN)-γ, in part produced by cardiac-infiltrating T cells.8 In contrast, previous studies have indicated a predominant Th2-type immune response in Balb/c mice, with low cardiac expression of IFN-γ and elevated IL4, leading to DCM in response to chronic arterial hypertension.15 Potentially, this immune phenotype of low IFN-γ and elevated IL1β in the heart of Balb/c mice may have been conductive to the robust lymphangiogenic response observed following pressure-overload. The gene discussed is IL4; the disease is myocardial infarction.