Interestingly, AhR−/- mice present vascular alterations, cardiomyocyte dysfunction, cardiomegaly and lymphocytic infiltrates,40 as well as augmented transforming growth factor (TGF)-β1 and cardiac fibrosis,41 and cardiomyocyte-specific deletion of its nuclear translocator, Ahrnt, results in cardiomyopathy.42 Our results also indicate that in mice protected from systolic dysfunction in response to TAC by either microbiota depletion, or genetic deficiency of T cells, AhR is not downregulated in response to TAC. The gene discussed is AHR; the disease is cardiomyopathy.