In prostate cancer, for example, GLS expression is enhanced by the oncogenic c-Myc, which positively regulates glutamine metabolism through the suppression of miR-23A/B [11], while in HCC the HOTTIP lncRNA, deregulated by miR-192 and miR-204, enhances the production of GLS1, determining the presence of abnormal glutaminolysis [57]. The gene discussed is GLS; the disease is Familial prostate cancer.