IMMP2L encodes the inner mitochondrial membrane peptidase subunit 2-like protein, which catalyzes the removal of transit peptides required for targeting proteins from the mitochondrial matrix across the inner membrane into the inter-membrane space. The protein plays a crucial role in mitochondrial protein processing and is known to process nuclear-encoded proteins like DIABLO. IMMP2L has emerged as a candidate gene for several neurodevelopmental disorders. Originally associated with Gilles de la Tourette syndrome through chr7 breakpoint disruption 1, subsequent studies have investigated its role in autism spectrum disorder (ASD), though a comprehensive meta-analysis found no significant association between IMMP2L deletions and ASD 2. However, differential DNA methylation of IMMP2L in families with 7q31.1 microdeletions has been associated with intellectual disability and developmental delay, suggesting epigenetic mechanisms may influence phenotypic penetrance 3. Recent research has implicated IMMP2L in schizophrenia subtypes characterized by enhanced glycation stress, where exonic deletions were found in patients with additional autistic features 4. The gene's disrupted function appears to cause glycation/oxidative stress in neuronal cells in an age-dependent manner, highlighting its importance in mitochondrial homeostasis and neurological health.