Because IFN-γ is profibrotic in TAC, as well as in Angiotensin II-induced hypertension, in which T cells also contribute to cardiac remodeling (Han et al., 2012), it is possible that the observed lack of fibrosis in CD43−/− TAC hearts is a result of this mechanism rather than a direct effect of CD43 in T cell recruitment across the myocardial vessels. The gene discussed is IFNG; the disease is persistent truncus arteriosus.