In this model, a subset of monocytes characterized as CD11b+Ly6C+ [classical monocytes (C-MOs)] preferentially migrates to the tumor-challenged lung via a chemokine receptor CCR2, and inhibition of their recruitment results in the reduction of the number of MAMs (CD11bhighLy6Clow) and metastatic tumor load in the lung (20). This evidence concerns the gene ITGAM and neoplasm.