The EMT-associated transcription factor, Dlx-2, was found to be responsible for mediating TGFβ- and Wnt signaling-induced GLS1 expression, whereas the perturbation of the glutamine metabolism by GLS1 silencing, glutamine starvation, and the use of inhibitors could arrest EMT (by regulating Snail expression levels), thereby suppressing tumor growth and metastasis [89]. This evidence concerns the gene GLS and neoplasm.