PINK1 overexpression partially restores mitophagy in HD models, indicating that compensatory pathways may bypass some mHTT-induced defects.222 Interestingly, regional analysis of Pink1-deficient models reveals striking neuroanatomical heterogeneity in mitophagic activity,223 implying that differences in neuronal susceptibility may stem from distinct reliance on Parkin-dependent versus alternative mitochondrial clearance mechanisms under varying physiological conditions. This evidence concerns the gene PINK1 and Huntington disease.