Pathway analyses highlighted membrane-proximal processes (external plasma membrane and IgG binding) and a 16p11.2 signal.<h4>Conclusion</h4>This integrative analysis identified <i>CCR2</i>-<i>ARTN</i> as a mechanistically supported immune-inflammation axis contributing to AML risk, offering a potential therapeutic target and warrants direct validation in primary <i>CD62L</i> <sup>+</sup> myeloid DCs. This evidence concerns the gene SELL and acute myeloid leukemia.