Further, ectopic expression of ST3GAL1 in melanoma cells increased the phosphorylation of AXL at residue Tyr702 in the catalytic kinase domain (Fig. 7f), which becomes autophosphorylated in response to AXL activation29, suggesting that ST3GAL1-mediated increased sialylation of AXL could be responsible for its activation. The gene discussed is AXL; the disease is melanoma.