Emerging evidence highlights the role of hepatokines (fetuin-A, FABP4) and inflammatory cytokines (TNF-α, IL-6) in creating a vicious cycle of progressive liver and kidney injury through lipotoxicity, endothelial dysfunction, and fibrotic signaling pathways [20–22] and create a pro-inflammatory milieu damaging both organs [23]. The gene discussed is IL6; the disease is endothelial dysfunction.