Allosteric activation of CD11b using two orthogonal approaches, pharmacologic (using GB1275) and genetic (using a I332G CD11b knock-in), provides significant reductions in the recruitment of F4/80+ TAMs in the TME and, concomitantly, results in significant decrease in tumor burden in LLC murine models, which is consistent with our previous results in other model systems (32, 34, 35). The gene discussed is ITGAM; the disease is neoplasm.