Conceptually, α-MG may target the STING pathway in endothelial, epithelial, or immune cells for circulating CCL5/CXCL10-mediated NK activation, leading to pre-injured lung vasculature and enhanced vessel permeability, which facilitates the entering of circulating tumor cells into the lung parenchyma and metastatic development. The gene discussed is CCL5; the disease is neoplasm.