The seemingly paradoxical effects of PS, in that it, on one hand, inactivates PI3K/AKT signaling to induce apoptosis of adherent tumor cells [6] and, on the other hand, activates PI3K/AKT signaling to suppress polyFN assembly on CTCs [49], can be reconciled by the fact that extracellular microenvironments between adherent tumor cells and CTCs are entirely distinct [9]. This evidence concerns the gene AKT1 and neoplasm.