Among the lipid‐independent effects, Niaspan is also thought to increase synaptic plasticity either directly, by promoting BDNF (brain‐derived neurotrophic factor) and TrkB (tyrosine receptor kinase) expression and function in neurons, or indirectly through HDL (Chen et al, 2014), suggesting a potential beneficial effect in regeneration and repair, which is a relevant clinical aspect in CMT. This evidence concerns the gene NTRK1 and Charcot-Marie-Tooth disease.