Inhibition of N-glycosylation with tunicamycin disrupts RTK signaling in tumor cells and enhances susceptibility of lung cancer cells to a therapeutic agent, erlotinib, emphasizing the importance of DPAGT1/N-glycosylation in RTK signaling in cancer (Contessa et al. 2008; Ling et al. 2009). This evidence concerns the gene DPAGT1 and cancer.