Beyond its serotonergic modulation, preclinical evidence indicates that vortioxetine suppresses pro-inflammatory cytokines (e.g., IL-6, TNF-α) through 5-HT3 receptor antagonism and enhances synaptic plasticity via 5-HT1A receptor agonism, both mechanisms implicated in post-stroke recovery (Krupa et al., 2023). The gene discussed is TNF; the disease is Stroke.