The treatment of LF cells with IGF-1 induced the phosphorylation of AKT and S6 which were blocked by the IGF-1R specific inhibitor, NVP-AEW541, and the mammalian target of the rapamycin C1 (mTORC1) specific inhibitor, rapamycin, suggesting the involvement of IGF-1 in the pathogenesis of LF hypertrophy via AKT/mTOR signaling [58]. This evidence concerns the gene IGF1R and Lassa fever.