BRINP1 (BMP/retinoic acid inducible neural specific 1) is a neural-specific protein expressed widely throughout the mammalian brain during development and adulthood 1. Its primary function is to suppress cell cycle progression in postmitotic neurons by inhibiting G1/S transition 2, and it plays a critical role in regulating neurogenesis and neuronal differentiation 3. Mechanistically, BRINP1 expression is regulated by neuron-restrictive silencing elements (NRSE) and DNA methylation patterns that establish neural-specific expression 4. Its expression is activity-dependent, particularly in the hippocampal dentate gyrus 3. BRINP1 deletion causes significant neurobiological abnormalities with psychiatric relevance. BRINP1-knockout mice exhibit increased hippocampal and cortical neurogenesis, altered parvalbumin-expressing interneuron populations, and behavioral phenotypes resembling autism spectrum disorder (ASD), attention-deficit/hyperactivity disorder (ADHD), and schizophrenia, including hyperactivity, reduced anxiety, poor social interaction, and memory impairment 35. Notably, BRINP1-deficient mice show decreased parvalbumin and somatostatin-expressing neurons in the medial prefrontal cortex, suggesting dysregulation of cortical excitatory/inhibitory balance 6. Clinically, BRINP1 hypermethylation is associated with maternal anxiety and depression during pregnancy 7, and genetic variants at the BRINP1 locus have been implicated in neurodevelopmental disorders 8, suggesting potential involvement in psychiatric disorder etiology.