At the same time, Roberts et al. described the preclinical pharmacology of the novel 5-HT3R partial agonist CSTI-300 in that decreasing the activity of the receptor evoked by the endogenous 5-HT could have a potential role in treating some of the symptoms of CS with a predicted reduced side-effect profile in comparison to telotristat and 5-HT3R antagonists. This evidence concerns the gene HTR3A and Cowden syndrome 1.