In the first study, we showed that early chronic fluoxetine treatment restore autism-like behavioral abnormalities via excitatory synapse-related transcriptomic reprogramming in ASD-model mouse. We characterized that deletion of ARID1B caused ASD-like behavioral deficits through persistently decreased density of excitatory synapses starting juvenile stage. Pharmacological correction using early chronic fluoxetine treatment targeting first three weeks after birth successfully carried out long-lasing rescue effects on synaptic deficits and behavioral abnormalities. The other study, however, claimed inhibitory synaptic dysfunction as main synaptic phenotype of Arid1b deletion using another mutant mice carrying same exon 5 deletion. In our recent work, by shifting genetic background of our Arid1b mutant mice, we highlighted that inhibitory synaptic dysfunction can be affected by genetic background. Moreover, we also showed that decreased excitatory synaptic transmission is a persistent phenotype of Arid1b haploinsufficiency regardless of the genetic backgrounds.