Indeed, both activated microglia, a major source of NO, and Th1-differentiated lymphocytes, consistent features of brain inflammation, release IL-1, IL-2, IL-6 and TNF-α, which in turn further contribute to glia activation, progression of inflammation and eventually cytotoxicity by an autocrine and paracrine process (Block and Hong 2007; Wei et al. 2014; Greenhalgh et al. 2020; Illes et al. 2020). The gene discussed is IL1B; the disease is brain inflammatory disease.