EMT activation has previously been proposed as the critical mechanism in the acquisition of a malignant phenotype by epithelial cancer cells; we now propose that the interaction between macrophages and apoptotic lung cancer cells can provide an anticancer microenvironment that inhibits EMT and the multistep process of cancer cell dissemination.42 First, our in vitro data demonstrate that ApoSQ-exposed CM from RAW cells and primary mouse BMDMs inhibits TGF-β1-induced EMT in 344SQ cells. The gene discussed is TGFB1; the disease is lung carcinoma.