In this study, along with the reduction of cell viability in vitro and tumor growth in vivo, the signaling transduction of IGF-1 R/p-PI3K/p-AKT/p-mTOR was abolished in ropivacaine-treated HepG2 cells and ropivacaine-challenged tumor-bearing mice in vivo. This evidence concerns the gene AKT1 and neoplasm.