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The proposed mechanisms are not all consistently supported by independent replication, and the molecular target(s) responsible for the observed effects have not been definitively identified

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It consists of a four-base pair deletion (c.401_404delTTCT, first reported as c.397_400delTTCT) in the MPTb domain, which causes a frameshift and premature termination of the protein (Phe134CysfsTer8) [73]

These findings suggest that restoring En2-regulated synaptic pruning or enhancing GABAergic synapse formation could rescue circuit imbalances in En2-associated ASD