In mice, inactivation of Brca2 (Brca2LoxP/LoxP; Nestin-cre) led to increased levels of yH2AX foci followed by apoptosis in both NPCs and early post-mitotic neurons, that culminates in defective neural development leading to microcephaly due to genotoxic stress. This evidence concerns the gene BRCA2 and microcephaly.