The reduction of cell viability by cilostazol, its synergism with KIT inhibition by STI-571 and the DNMDP cytotoxicity observed in GIST882 cells in vitro on one hand, and the broad expression of PDE3A and SLFN12 in human GIST tissue arrays on the other, make of PDE3A a novel appealing prospect in the ongoing quest for GIST targeted therapy. The gene discussed is SLFN12; the disease is gastrointestinal stromal tumor.