Although TGFβ-Receptor I (also known as ALK1) and SMAD-1/-5 pathway has previously been found to activate IGFBP7 expression in glioblastoma vascular and tumor endothelial cells where IGFBP7 plays a pro-angiogenic role [57], whether upregulation of SMAD-3 following treatment of MPM cells with DSF-Cu (Table 1) also caused elevated expression of IGFBP7, and to the extent this signaling contributed to MPM cell growth inhibition/apoptosis in the presence of DSF-Cu is intriguing and remains to be clarified. This evidence concerns the gene SMAD1 and neoplasm.