Our findings may also relate to studies that show rescue of synaptic and behavioral deficits in AD mouse models by knocking down the IGF-1 receptor and inhibiting the phosphoinositide three kinase (PI3K), which are upstream of Akt-HTT (Cohen et al., 2009; Humbert et al., 2002; Martínez-Mármol et al., 2019). The gene discussed is AKT1; the disease is Alzheimer disease.