It was reported that c-Myc could promote the proliferation of prostate cancer and B lymphoma cell lines by suppressing miR-23a/b and subsequently increasing the GLS1 expression level.16 In colon cancer, a lncRNA called CCAT2 that interacts with the CFIm complex fine-tunes the alternative splicing of glutaminase (GLS) by selecting the poly(A) site in intron 14 of the precursor mRNA, resulting in the preferential expression of the GAC isoform.17 In breast cancer cells, activated c-jun induced GLS expression by directly binding to the GLS promoter region. The gene discussed is JUN; the disease is breast carcinoma.