The expression of neuroligins or neurexins in cultured nonneuronal cells demonstrates that these molecules are sufficient to induce presynaptic specializations in mouse hippocampal neurons in vitro. Rare mutations in neuroglian and neurexin genes have been associated with familial autism spectrum disorders. However, even mice lacking all three neuroligin genes still have the normal number of synapses. Propose some possible explanations to reconcile these findings and suggest some experiments that could be performed to distinguish between them.