It was observed that sorafenib determined a dose-dependent inhibition of proliferation of GBM cells, also inducing autophagy and apoptosis, and inhibited the phosphorylation of signal transducer and activator of transcription 3 (Stat3), but also the expression of cyclins D and E. It was able to reduce angiogenesis, and was well tolerated [110]. This evidence concerns the gene STAT3 and glioblastoma.