Maternal immune activation during COVID-19, driven by elevated IL-6, IL-8, TNF-α, and other pro-inflammatory mediators such as IL-1β, disrupts foetal neurodevelopment by priming microglia, altering dopaminergic/γ-aminobutyric acidergic (GABAergic) pathways, and activating complement cascades. The gene discussed is IL6; the disease is COVID-19.