Our previous study in fibroblasts from patients with CMT2P showed that C694R mutation disrupts the protein–protein interactions between LRSAM1 and RNA-binding proteins (including FUS and G3BP1), leading to altered nuclear-cytoplasmic translocation of the RNA-binding proteins, a potential mechanism of neuronal degeneration in CMT2P6. This evidence concerns the gene G3BP1 and Charcot-Marie-Tooth disease axonal type 2P.