GLS and neoplasm: Inhibition of glutaminolysis by Gln depletion, by chemical inhibition of the critical regulators of Gln metabolism such as GLS and MYC, or genetic knockdown of these genes and Gln transporters resulted in the inhibition of the essential CSC-driving signaling mechanisms (e.g., WNT/β-catenin; oxidative stress response; DNA damage response), CSC depletion in vitro and in vivo, and tumor radiosensitization [6].