This nutrient imbalance triggers chronic activation of innate immune pathways and promotes the systemic release of pro-inflammatory cytokines such as Interleukin-6 (IL-6), Tumor Necrosis Factor alpha (TNF-α), and Interleukin-1 beta (IL-1β), all of which are implicated in airway inflammation, hyperresponsiveness, and tissue remodeling, central features of asthma pathophysiology [39,40]. The gene discussed is TNF; the disease is inflammation.