How the extra copy of PMP22-caused diseases is not fully understood, but studies in rodent models as well as in CMT1A patient–derived fibroblast show that PMP22 can form cytosolic aggregates accompanied by reduced proteasomal activity, which may ultimately lead to cytotoxicity [9–11]. The gene discussed is PMP22; the disease is Charcot-Marie-Tooth disease type 1A.