ATP5PB encodes the peripheral stalk-membrane subunit b of mitochondrial ATP synthase (Complex V), a critical component of the F(0) domain that functions as a stator to maintain the catalytic core stationary relative to rotating elements 1. This subunit is essential for coupling proton translocation across the inner mitochondrial membrane to ATP synthesis via a rotary mechanism 1. ATP5PB expression is dynamically regulated in response to metabolic and environmental stress. Elevated ATP5PB expression is associated with poor survival outcomes in acute myeloid leukemia patients with CEBPA bZIP mutations, suggesting dysregulated mitochondrial metabolism correlates with leukemic progression 2. Environmental stressors impair ATP5PB function: exposure to the automotive pollutant 6PPDQ causes covalent binding to ATP5PB, reducing Complex I and IV activities by ~25% and cellular ATP by ~20% 3. Similarly, ammonia exposure alters ATP5PB expression and acetylation, disrupting mitochondrial energy metabolism and contributing to pulmonary fibrosis pathology 4. ATP5PB protein levels also change in response to immune modulators like chlorhexidine in macrophages 5. These findings establish ATP5PB as a sensitive indicator of mitochondrial dysfunction in disease states and environmental toxicology.