One can speculate if the variants in TNNT2 alone are responsible for the aggressive phenotype in the young girl in our family or the prenatal case in the family presented by Van Acker et al.; is it possible to explain this by another modulating variants in another part of the genome or did the infectious disease in the index patient act as a trigger event for the underlying hereditary cardiomyopathy? The gene discussed is TNNT2; the disease is infectious disease.