Scientists discovered a novel self-perpetuating cancer mechanism in the lung microenvironment, wherein EGFR-driven lung adenocarcinoma cells exploit lung-resident macrophages — remodeling them to provide nutrients, like cholesterol, to the cancer cells and stimulate tumor growth. Their findings provide new inspiration for lung adenocarcinoma interventions that disrupt this tumor cell-macrophage relationship, as well as suggest that existing EGFR inhibitor treatments may be more successful if paired with statins.