METTL13 is a dual methyltransferase that catalyzes two distinct methylation reactions on elongation factor 1-alpha (eEF1A1 and eEF1A2): via its C-terminus it methylates the N-terminal Gly-2 residue, while via its N-terminus it dimethylates lysine 55 1. These methylations increase eEF1A's intrinsic GTPase activity and enhance protein synthesis output 2. METTL13-mediated eEF1AK55me2 modification modulates codon-specific translation rates 1. Disease relevance is context-dependent: in Ras-driven cancers (pancreatic and lung), METTL13 is upregulated and promotes tumorigenesis; METTL13 deletion reduces neoplastic growth and sensitizes tumors to growth-pathway inhibitors 2. Conversely, METTL13 is downregulated in bladder cancer where it functions as a tumor suppressor, inhibiting cell proliferation and invasion 3. In breast cancer, eEF1A2 exhibits tumor-suppressor functions when bound to PTEN rather than METTL13 4. METTL13 is required for T-ALL cell proliferation and associates with high-risk pediatric leukemia 5. Additionally, a METTL13 modifier variant suppresses GAB1-associated deafness through MET signaling modulation 6. METTL13 represents a promising therapeutic target whose inhibition may constitute a specific vulnerability in Ras-driven cancers.