Finally, considering evolutionary conservation of RPTPs, as well as the conservation of POMTs, our findings suggest that mammalian RPTPs, such as RPTPζ and possibly other RPTPs, are also substrates of POMTs, and that POMTs are important effectors of RPTP functions in mammalian organisms, which may underpin neurological defects of dystroglycanopathies caused by POMT mutations. The gene discussed is PTPRS; the disease is neuromuscular disease caused by qualitative or quantitative defects of alpha-dystroglycan.