In I/R–AKI, SHED treatment attenuated renal infiltration of macrophages/neutrophils and reduced MCP-1, MIP-2 and IL-1β in vivo, while SHED-CM suppressed MCP-1 production in tubular epithelial cells, consistent with a paracrine anti-inflammatory effect in the kidney [23]. The gene discussed is IL1B; the disease is acute kidney injury.