Previous studies have shown that early spontaneous activity patterns are altered in the neocortex of animal models of neurodevelopmental disorders such as the Fmr1 knock out model of Fragile X syndrome (FXS; Cheyne et al., 2019) and the Nr2f1-deficient model of Bosch-Boonstra-Schaaf optic atrophy syndrome (Del Pino et al., 2020) suggesting a link between the early generation of spontaneous activity and abnormal brain development. This evidence concerns the gene NR2F1 and fragile X syndrome.