Together, these findings implicate liver-derived pro-inflammatory cytokines (IL-1, IL-6, TNF-α), extrinsic apoptosis signaling (TNF-α/TNFSF), and metabolic oxidative stress (e.g., ROS) as circulating drivers that initiate and amplify AKI in the context of fatty liver IRI. The gene discussed is IL1A; the disease is acute kidney injury.