This study investigates the reversibility of neurological defects in a mouse model of Rett Syndrome (RTT), an autism spectrum disorder caused by mosaic expression of mutant *MECP2* genes in neurons. The researchers created a mouse model where the *Mecp2* gene is conditionally deleted and can be reactivated using tamoxifen (TM). They found that reactivating *Mecp2* expression in both immature and mature adult animals led to a significant reduction in advanced neurological symptoms. The study demonstrates that viable but defective neurons can be repaired, suggesting that the damage caused by the absence of MeCP2 during development may not be irreversible. The results also show that late-onset neurological symptoms in mature adult mice can be reversed by restoring MeCP2 expression. Additionally, the study found that long-term potentiation (LTP) deficits in *Mecp2*-deficient mice are reversible, further supporting the reversibility of RTT-like neurological defects. These findings suggest that RTT may not be a strictly neurodegenerative disorder and open the possibility for therapeutic interventions in related human disorders.This study investigates the reversibility of neurological defects in a mouse model of Rett Syndrome (RTT), an autism spectrum disorder caused by mosaic expression of mutant *MECP2* genes in neurons. The researchers created a mouse model where the *Mecp2* gene is conditionally deleted and can be reactivated using tamoxifen (TM). They found that reactivating *Mecp2* expression in both immature and mature adult animals led to a significant reduction in advanced neurological symptoms. The study demonstrates that viable but defective neurons can be repaired, suggesting that the damage caused by the absence of MeCP2 during development may not be irreversible. The results also show that late-onset neurological symptoms in mature adult mice can be reversed by restoring MeCP2 expression. Additionally, the study found that long-term potentiation (LTP) deficits in *Mecp2*-deficient mice are reversible, further supporting the reversibility of RTT-like neurological defects. These findings suggest that RTT may not be a strictly neurodegenerative disorder and open the possibility for therapeutic interventions in related human disorders.