DES and hydrops fetalis: Also, the enhanced activity of the post-translational modifications or mutations of the N-terminal domain of desmin [40] may cause the misfolding of this intermediate filament, further disrupting the organizational compartments of sarcomeric components [34] and producing pro-amyloidogenic oligomers [12,40], which may become a source for protein aggregate formation, thus contributing to direct toxic cellular injury and altering the overall mechanics of the sarcomeric component of the cardiomyocytes in the symptomatic ischemic HF irreversibly [37,41].