Because established BM contain considerable inflammatory infiltrates composed of various immune cells [44], the marked reduction of the large peritumoral edema on progressive NSCLC BM might reflect how silibinin-induced inhibition of STAT3 may increase the immunogenicity of BM cancer cells via cell-autonomous pathways and/or may favor the cell-nonautonomous reprogramming of the BM microenvironment (e.g., endothelial cells, tumor-associated macrophages, tumor-infiltrating lymphocytes) toward an immunostimulatory state [45–48]. This evidence concerns the gene STAT3 and neoplasm.