Interestingly, the hyper-N-glycosylated GRP94 at the PM contributed to the stability of GRP94-receptor tyrosine kinase complexes, which indicates that GRP94 can adopt a unique hyperglycosylated conformation to preferentially regulate growth factor receptors on tumor cells and alter tumor oncogenesis (66) (Figure 1A). The gene discussed is NTRK1; the disease is neoplasm.