STAMBP and microcephaly: Ishii et al. (2001) reported that Stambp-deficient mice were morphologically indistinguishable from their littermates at birth and assumed that apoptotic activation was the major pathogenic mechanism of STAMBP mutation. Although mouse models can capture some clinical features of human conditions, human organoids provide unique functions in the study of human diseases and complement animal models. The pathophysiological mechanism that associates STAMBP mutations with microcephaly needs to be studied using multiple suitable models.