Previous studies in Drosophila have shown that GCN2 (eIF2AK4) and PERK (eIF2AK3) can cooperate to modulate FOXO activity in response to ER stress (You et al., 2018; Zhang et al., 2013), suggesting the PERK-related GCN2 can potentially compensate for the inactivation of PERK function in cancer cells. The gene discussed is EIF2AK3; the disease is cancer.