To understand the molecular underpinnings of RTT, mice lacking Mecp2 or carrying RTT-associated mutations in Mecp2 have been developed, and the majority of clinical features are observed in these whole-body Mecp2-mutant mice, such as normal development during early life followed by symptomatic presentation of altered gait, motor incoordination, hindlimb clasping, and cognitive deficits [91,92,93]. The gene discussed is MECP2; the disease is Cognitive impairment.