This could include several genes mutated in different forms of CMT (e.g., NEFL, RAB7A, FGD4, FIG4, SH3TC2, LITAF/SIMPLE) (reviewed in [83]) encoding proteins regulating PIs metabolism and membrane trafficking; and myopathies involving mutations in caveolin 3 and dysferlin genes, which also lead to common defects in T-tubules and membrane transport in patients and animal models (Figure 3) [84], . Here, RAB7A is linked to myopathy.