We propose that curcumin exerts its broad therapeutic effects via a unified “inflammation–oxidative stress axis”, primarily by inhibiting NF-κB and NLRP3 activation, reducing ROS and pro-inflammatory cytokines (TNF-α, IL-1β/18), as seen across models of depression, metabolic disorders, and neurodegeneration. The gene discussed is IL1B; the disease is depressive symptom measurement.