Functional evidence for in vivo significance of these interactions comes from genetic studies in humans that show that mutations of either the catalytically active MTMR2 or its catalytically inactive binding partner MTMR13 result in similar forms of Charcot-Marie-Tooth disease [23], [24], [25], [26]. The gene discussed is MTMR2; the disease is Charcot-Marie-Tooth disease.