The latter suggests that Cav-2 deficiency in the non-malignant cell types of the tumor microenvironment initiates a robust anti-tumor immune response to lung carcinoma mediated via increased infiltration and activation of M1-polarized macrophages, subsequent attraction of cytotoxic CD8 T cells into tumors, and tumor eradication in mice. The gene discussed is CAV2; the disease is lung carcinoma.