Post-translational modifications lie at the heart of cell signaling research field. Notably, the PI3K/Akt/mTOR signaling pathway is one of the primarily dysregulated pathways that associates with most hallmarks of cancer, such as sustaining proliferative signaling and metabolic reprograming. We are interested in understanding whether and how arginine methylation regulates the PI3K/Akt/mTOR proliferative pathway and cell metabolism. For example, we characterized that PRMT5 specifically catalyzes symmetric dimethylation of Akt1 to promote growth factors induced Akt activation and tumor growth (Yin et al. Nature Communications, 2021), while PRMT1 promotes amino acids induced mTORC1 pathway activation by methylating WDR24 (Yin et al. Cell Reports, 2023). We also demonstrated that Hippo pathway-mediated inactivation of mTORC1 suppresses glycolysis and lipid biosynthesis (Gan et al. Nature Cell Biology, 2020).