The severity of experimental sepsis, as reflected by the systemic accumulation of a panel of surrogate markers (e.g., interleukin [IL-6], KC, monocyte chemoattractant protein-1 [MCP-1], and granulocyte-colony stimulating factor [G-CSF]) and parallel animal mortality, can be artificially controlled by varying the size of the needle used to puncture the cecum (3). This evidence concerns the gene CCL2 and Sepsis.