Interestingly, the P0T124A and P0N122S mutations, which similarly abolish native N-glycosylation, are responsible for late-onset CMT1B with only moderate reduction of NCV [7,68,69], and like P0T124M, these mutated P0 proteins retain their adhesive propriety in vitro [70]. The gene discussed is MPZ; the disease is Charcot-Marie-Tooth disease type 1B.