In contrast, the three other XLCNM patient mutants MTM1V49F, MTM1R69C and MTM1N180K showed PtdIns3P phosphatase activity comparable to the wild-type MTM1, as they displayed a strong decrease in the PtdIns3P levels which represented only 45–50% of total PtdInsP (Figure 4A). This evidence concerns the gene MTM1 and X-linked myotubular myopathy.