Despite an enhanced corticolimbic release of acetylcholine, glutamate, and monoamines that favors cognitive processes [19], the disrupted recruitment of mechanistic target of rapamycin (mTOR) signaling that occurs upon HTR6 inhibition is postulated as a mechanism mitigating cognitive deficits in animal models of schizophrenia [20]. Here, MTOR is linked to schizophrenia.