Several genetic forms of CMT have been described with abnormal myelin histopathology and tomacula formation (CMT4B, CMT4H, CMT4F, CMT1B, and HNPP).1 The causative proteins contain phosphoinositide binding domains in CMT2B/RAB7, CMT4B1/MTMR2, CMT4B2/SBF2, CMT4J/FIG4, and CMT4H/FGD4, suggesting that abnormal PI(3)K signaling is a common final pathway in demyelinating CMT (figure 2E). This evidence concerns the gene RAB7A and Charcot-Marie-Tooth disease.