However, analysis of tumor nodules from mice receiving a 5-day sorafenib treatment revealed a marked reduction of tumor angiogenesis, eventually associated with inhibition of vascular phospho-Akt and/or phospho-ERK1/2, thus suggesting that inhibition of angiogenesis is likely to play a key role in triggering the antitumor activity of sorafenib. This evidence concerns the gene AKT1 and neoplasm.