Furthermore, when glutamine catabolism is inactivated, tumor cells can produce glutamate via asparagine synthetase (ASNS)-mediated glutamine, which in turn can generate ATP, thereby inhibiting the AMPK pathway and completely activating mTORC1 on the lysosomal surface, a process primarily mediated by the mTORC1 coactivator Rheb [144]. The gene discussed is ASNS; the disease is neoplasm.