AKT activation of SREBP1 by multiple mechanisms regulates lipid metabolism in some malignancies, such as breast cancer, glioblastoma, and melanoma, making SREBP1 driven by overactive AKT a novel antitumor target to explore.23, 24, 25 Liu et al demonstrated that AKT was overexpressed in lung adenocarcinoma and positively correlated with SREBP1-SDMA, and AKT signaling activation could affect ubiquitin-protease degradation of SDMA-modified SREBP1, thereby increasing the stability of PRMT5-mediated mSREBP1 protein.26 This evidence concerns the gene SREBF1 and glioblastoma.