Indeed, a recent study of a knock-in model of mutant Hsp27, in which the mutant protein is expressed at physiological levels, failed to show any motor deficits or any signs of axonal abnormalities (21), leading the authors to conclude that expression of the mutant protein at physiological levels is insufficient to induce CMT-2 pathology within the lifespan of the mouse, at least at the system level. Here, HSPB1 is linked to Charcot-Marie-Tooth disease type 2.