These findings, in combination with the reduced angiogenesis observed in myeloid MK2 knock-out animals, which is fully restored by adoptive transfer of MK2 WT macrophages into animals lacking MK2 in the myeloid compartment, strongly implicates the macrophage MK2-Cxcl-12 axis as a critical regulator of tumor neo-angiogenesis, consistent with the known role of Cxcl-12 in tumor promotion and vascularization (48, 49). Here, MAPKAPK2 is linked to neoplasm.