Despite recent advances in understanding the molecular mechanisms of autism 
spectrum disorders (ASD), the current treatments for these disorders are mostly 
focused on behavioral and educational approaches. The considerable clinical and 
molecular heterogeneity of ASD present a significant challenge to the 
development of an effective treatment targeting underlying molecular defects. 
Deficiency of SHANK family genes causing ASD represent an exciting opportunity 
for developing molecular therapies because of strong genetic evidence for SHANK 
as causative genes in ASD and the availability of a panel of Shank mutant mouse 
models. In this article, we review the literature suggesting the potential for 
developing therapies based on molecular characteristics and discuss several 
exciting themes that are emerging from studying Shank mutant mice at the 
molecular level and in terms of synaptic function.