AKT1 and Kaposi's sarcoma: vGPCR directly leads to the overactivation of the PI3K/AKT/mTOR pathway that is necessary for KSHV-induced transformation of endothelial cells to KS spindle cells.115, 127 In addition, vGPCR activation of MTORC1 leads to secretion of pro-angiogenic factors causing paracrine signaling, which recruits and stimulates other non KSHV infected cells.127 As a result, mTOR inhibition has been used more successfully in the clinic for KS.