We have recently demonstrated that the irreversible ERBB1/2/4 inhibitor neratinib could down-regulate the expression of RAS proteins, and based on this data and the fact that phosphorylated fingolimod causes sphingosine-1-phosphate receptor 1 internalization and degradation, we wished to determine whether this drug could act upon RAS proteins in GBM cells, in a manner similar to neratinib (20, 21, 24, 31). This evidence concerns the gene S1PR1 and glioblastoma.