In addition to the lack of viability of Gemin5 KO in these animal model systems, it has been recently shown that GEMIN5 biallelic variants lead to a spectrum of neurodevelopmental diseases that occur to different degrees (Kour et al. 2021; Francisco‐Velilla, Embarc‐Buh, del Caño‐Ochoa et al. 2022; Saida et al. 2021; Zhang et al. 2023; Ibrahim et al. 2023; Cascajo‐Almenara et al. 2024; Zhang et al. 2024), often resulting in neurodevelopmental delay, hypotonia, and cerebellar ataxia (reviewed in Nelson and Pandey 2024). Here, GEMIN5 is linked to aceruloplasminemia.