I am analyzing a dataset and one of the patients has a LoF function mutation on the 5HTR2B gene (stopgain). I've looked at a few studies indicating a variety of patterns in 5HTR2B knockout mice:
"Mice Lacking the Serotonin Htr2B Receptor Gene Present an Antipsychotic-Sensitive Schizophrenic-Like Phenotype."
https://www.ncbi.nlm.nih.gov/pubmed/25936642
"5-HT2B receptors are required for serotonin-selective antidepressant actions"
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3381222/
I don't know enough about the development of these receptors to understand what impact there would be on a real person. Would the second copy of the gene from the other parent compensate, or would the person end up with 50% fewer receptors? I do know studies showing a premature stop-codon in human populations increases severe impulsivity: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3183507/
I do not think that this can be answered without further data. Depends on how that gene is regulated, the cellular context and the function of the protein. Maybe the reduced levels are sufficient in a standard situation while under cellular stress one would observe a notable phenotype. Would probably need to be investigated by experiment.