Fingolimod is a well known immunomodulator used by oral route in relapsing multiple sclerosis patients. Upon phosphorylation by sphingosine kinase 2 (SPHK2), fingolimod binds to one or more of at least five G protein coupled receptors known as S1PR1-5, thus it causes S1PRs internalization and consequent sequestration of lymphocytes in lymphoid organs. Fingolimod also affects other signaling pathways. In particular, this drug is able to activate the serine-threonine protein phosphatase 2A (PP2A) which regulates multiple cell signaling cascades by virtue of its phosphatase activity. PP2A loss-of-function may represent one of the major events contributing to cancer development and progression. Hence, there is a need for therapeutic PP2A reactivation. In this regard, fingolimod is revealing a promising candidate for cancer treatment due to its ability to reactivate PP2A, reduce cell viability and promote apoptosis. However, the appropriate dosage and safety remain a challenge.