In human liposarcoma models, overexpression of the phosphorylation-mimetic mutant (METTL1-S27D) significantly compromised methyltransferase function yet effectively cooperated with AKT to drive sarcomagenesis, and the catalytically dead mutant (L160A/D163A) similarly retained oncogenic potential, confirming that METTL1-mediated tumor promotion operates independently of its methyltransferase activity. The gene discussed is METTL1; the disease is liposarcoma.