Thus, while systemic administration of a TLR9 agonist inhibited cardiac hypertrophy and dysfunction in isoproterenol and pressure overload-induced cardiomyopathy [3,17], TLR9 activation restricted to the cardiomyocyte leads to aggravated HF, this noteworthy also in pressure overload induced cardiomyopathy [2]. The gene discussed is TLR9; the disease is hydrops fetalis.