Indeed, in vivo study in dystroglycanopathy mouse model with FKRP mutations confirms that ribitol treatment is able to increase the levels of CDP-ribitol and partially restore the hypoglycosylation of α-DG in both skeletal and cardiac muscles with improvement in muscle functions25. Here, FKRP is linked to neuromuscular disease caused by qualitative or quantitative defects of alpha-dystroglycan.