In this scenario, the increased supply of acetylcholinesterase would degrade acetylcholine in the interneuronal junction faster, thus suppressing cholinergic signaling to a greater extent than in the brain with wildtype GABBR1. Figure 6A systematically depicts hypothesized impact of GABBR1’s autism-associated intronic variant on GABA-ergic and cholinergic signaling. This evidence concerns the gene ACHE and autism.