Indeed, partial inhibition of signaling downstream of PERK has proven effective at ameliorating NDD pathology without causing secondary toxicity (Halliday et al., 2015, 2017; Bugallo et al., 2020), and has also been demonstrated to ameliorate natural age-related cognitive decline in old mice (Krukowski et al., 2020), suggesting that fine-tuning PERK signaling as opposed to total inhibition may prove a better therapeutic strategy to target aging and age-related NDD. The gene discussed is EIF2AK3; the disease is Neurodevelopmental delay.