NPPB and Menkes disease: As discussed previously, one explanation for this observation may be that serum BNP levels are supposed to reflect rapid changes of pressure gradients in the atria and ventricles and one may argue that the underlying pathophysiology in MD patients is mainly driven by continuous myocardial cell death (due to dystrophin absence or fragility) resulting secondarily in a continuous and adapted ventricular enlargement with progressive decrease of systolic function, however, without quick changes in atrial/ventricular filling pressures [10, 26, 27].