Given the dependency of cancer cells on glutamine to support the energy and metabolite demand of the cancer cells and the concurrent activation of signaling pathways such as c-Myc [10] and K-Ras [11] in several cancer types, the possible activation of upstream signaling pathways/transcription factors might be a likely mechanism for the upregulation of SLC38A1 in OSCC. The gene discussed is MYC; the disease is cancer.