Whereas we recently proposed a mechanism by which endothelial cell ASMase/ceramide activation triggers a cascade of events that link in trans to tumor cell SSR-mediated inactivation of HRR (3), timed delivery of antiangiogenic drugs to optimally derepress VEGF-inhibited ASMase in tumor microvasculature (3, 22–24) should, if our concepts are correct, enhance SSR-induced HRR inactivation and improve tumor response. This evidence concerns the gene VEGFA and neoplasm.