To elucidate the molecular pathogenesis underlying microcephaly, we generated NSC‐restricted Eftud2 knockout murine models using hGFAP‐Cre‐mediated recombination, achieving targeted gene ablation from embryonic day 12.5 (E12.5).[35, 36] Comparative immunofluorescence and immunoblot analyses of neonatal cortices confirmed substantial Eftud2 depletion in hGFAP‐Cre; Eftud2f/f (Eftud2hGFAP) mice compared to controls (Eftud2f/f) (Figure S4B–D, Supporting Information), validating the successful establishment of NSC‐specific knockout lineages. Here, EFTUD2 is linked to microcephaly.