The regulation of both, mTORC1 and glutaminolysis suggests that mTORC1 and glutaminolysis act in both directions hence they are found to regulate each other for promoting cell growth and cancer progression; mTORC1 also induces glutaminolysis by activating c-MYC-GLS and because c-MYC is GLS and GLUD1 transcription factor, glutamine metabolism is favored; additionally, the glutaminolysis-mediated activation of mTORC1 participates in autophagy inhibition and the DNA double-strand breaks sensor serine/threonine protein kinase ATM which participates in cell cycle delay after DNA damage. Here, MYC is linked to cancer.