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GABAergic cell loss in mice lacking autism-associated gene Sema6A biorxiv.org/content/10.110… - loads of interesting anatomical + behavioral defects in these mutants, but no strong evidence for association with autism, IMO 
Given the profile of defects observed in Sema6a mutant mice it wouldn't be surprising if mutations in humans (in this or interacting genes like Plexins) were associated with neurodevelopmental disorders...
And a few patients with various psychiatric conditions (notably SCZ + ASD) have been found to carry such mutations but their pathogenicity is not proven.
Mutation of Semaphorin-6A disrupts limbic and cortical connectivity and models neurodevelopmental psychopathology. ncbi.nlm.nih.gov/pubmed/22132072
This paper of ours showed many anatomical defects across multiple brain systems in Sema6A mutant mice, with emergent pathophysiological and behavioral disturbances...
Some of those emergent states shared pharmacological characteristics with psychosis in humans: they were made worse by amphetamine and improved by clozapine
We think of these states not as direct consequences of any particular anatomical phenotype but as the outcome of maladaptive reactive processes of brain development which can probably be induced by diverse neurodevelopmental insults
In other words, we don't think there's anything special about Sema6A - mutations in many, many different can kick the developing brain into a trajectory towards a pathophysiological end-state
