Taken together, these observations strongly suggest that perturbations in neurofibromin-MEK-ERK signaling promote myeloid-cell mediated VSMC proliferation and arterial stenosis, but little is known about the interaction between discrete myeloid subpopulations and VSMCs and whether targeting individual populations is advantageous to prevent or treat NF1 arteriopathy. Here, NF1 is linked to neurofibromatosis type 1.