They are vital for the study of enzyme kinetics and enzyme inhibition. This causes cortical activation and thus a movement inhibition. They are about at least 10-fold selective for inhibition of serotonin reuptake over norepinephrine reuptake. It is highly selective in its inhibition of serotonin reuptake. This is indicative of the positive correlation between behavioral inhibition and selective mutism. This results in the inhibition of prostaglandin synthesis. Additional mechanisms of action such as inhibition of monoamine reuptake may be involved also. This indicates minimal inhibition of aromatase by ketoconazole "in vivo" in humans. No reuptake inhibition of any of the neurotransmitters occurs. After prolonged exposure to high fatty acid concentrations this changes to an inhibition. This pathway is regulated by product inhibition. It works by preventing bacteria from reproducing through the inhibition of protein synthesis. It has approximately 106-fold selectivity for COX-2 inhibition over COX-1. In a 2016 study, the relationship between behavioral inhibition and selective mutism was investigated. This behavior occurs due to unilateral growth inhibition.