In AML, LANs’ functional role is unclear, but an FGFR1-driven murine model revealed leukemogenesis polarizes neutrophils into six subsets (notably Ly6g+ and Camk1d+), which upregulate MMP8/9 to migrate from bone marrow to blood and differentiate into PMN-MDSCs; MMP inhibition with Ilomastat blocked migration and improved survival, while clinical data linked high MMP8 to poor AML outcomes, highlighting MMP8 as a potential therapeutic target to disrupt immune evasion (177). Here, MMP8 is linked to acute myeloid leukemia.