Dajon et al., using a murine model of lung adenocarcinoma, found that stimulation of Toll-like receptor 7 (TLR7) expressed by adenocarcinoma cells modulated the immune infiltrate, leading to a significant expansion of MDSCs that was associated with increased secretion of CCL2 and GM-CSF in the tumor microenvironment. The gene discussed is CCL2; the disease is neoplasm.