In line with the immunometabolic hypothesis, studies have shown that genetic polymorphisms in inflammatory genes such as interleukin 1 beta (IL-1β), tumor necrosis factor alpha (TNFα) and C-reactive protein, influence depression incidence, severity, and treatment response (Barnes et al., 2017; de Kluiver et al., 2019, 2021; Draganov et al., 2019; Kappelmann et al., 2021). The gene discussed is IL1B; the disease is depressive symptom measurement.