Reduced β-arrestin levels in patients with depression would likely reduce both 5-HT1A and 5-HT2A endocytosis given their established interaction with β-arrestins (Della Rocca et al., 1999; Schmid et al., 2008), while β-arrestin rescue by antidepressant treatment would potentially restore 5-HT1A and 5-HT2A endocytosis rates. This evidence concerns the gene HTR2A and depressive symptom measurement.