In addition to inhibiting Bcr-Abl tyrosine kinase, it targets type III split domain tyrosine kinase family (c-kit, PDGFRA, FLT-3), thus inhibiting PDGFRA signaling.15–17 Preclinical data showed increased potency of nilotinib compared to first-generation imatinib in inhibiting the growth of human glioma cell lines and stem cells.18 These findings, together with evidence indicating less susceptibility to resistance via active cellular transporter pumps,19 we hypothesized that nilotinib might improve response in biomarker-enriched patients. This evidence concerns the gene PDGFRA and glioma.