Presence of the two fragments of 100 and 130 kDa in the sera of DMD patients as well as LGMD2D patients and in different animal models of DMD (mdx mouse, GRMD dog) and other forms of muscular dystrophy indicates a conserved mechanism of MYOM3 proteolysis and release across species and diseases. This evidence concerns the gene MYOM3 and autosomal recessive limb-girdle muscular dystrophy type 2D.