Differentiation-inducing factor (DIF) produced by Dictyostelium discoideum inhibits the growth, motility (migration and infiltration) and adhesion to endothelial cells of many types of cancer cells, which leads to the inhibition of cancer growth and metastasis. Its mechanism of action has long remained unclear, however recent studies have revealed that AMP-activated protein kinase (AMPK)-mediated inhibition of mTORC1 activity is the early signal of DIF. When mTORC1 is inhibited, S6 kinase is suppressed, resulting in the suppression of cell proliferation and cell motility through the suppression of STAT3 and Snail. And moreover, analysis of DIF-binding proteins has suggested that DIF binds to and inhibits type 2 malate dehydrogenase (MDH2), which may lead to the activation of AMPK. Although DIF synthase has not been found in organisms other than Dictyostelium, the target molecule MDH2 is conserved in almost all organisms. This is probably why the effects of DIF extend to mammals. Many drugs have been made from natural toxins, such as plant alkaloids, however drugs made from signal molecules of other organisms, such as DIF, are rare. In this talk, I would like to consider the possibility of clinical application of DIF.