A chronic treatment with first- and second-generation antidepressants rescues BDNF levels in different preclinical models of depression (Duman and Monteggia, 2006), while selective serotonin reuptake inhibitors (SSRIs) drugs and the new multimodal antidepressant vortioxetine are able to reverse the depressive-like phenotype and memory deficits induced by amyloid-β (Aβ) in mice by the rescue of TGF-β1 (Torrisi et al., 2019). The gene discussed is TGFB1; the disease is major depressive disorder.