In the context of cyst(e)inase treatment, GCN2 signaling appeared more important than signaling through AMP kinase (AMPK), another known inhibitor of mTORC1, because sustained AMPK activation was observed in only Panc1 cells even though mTORC1 was inhibited in all three cell lines (Fig. 2h). Here, EIF2AK4 is linked to cyst.