These enriched taxa are primarily pro-inflammatory organisms whose baseline presence may predispose to cytokine-mediated anemia through multiple interconnected mechanisms: pro-inflammatory cytokines such as IL-6, IL-1β, and TNF-α suppress erythropoiesis both by reducing erythropoietin production and by directly interfering with erythroid progenitor differentiation, while simultaneously inducing hepcidin expression that causes iron sequestration in macrophages and enterocytes, rendering iron unavailable for hemoglobin synthesis despite adequate stores [33,34,35]. The gene discussed is IL1B; the disease is anemia (phenotype).