AKAP10 is a mitochondrial and plasma membrane-anchoring protein that binds protein kinase A (PKA) regulatory subunits to facilitate localized PKA signaling. Its primary function involves anchoring PKA to mitochondria, where it phosphorylates and inactivates pro-apoptotic proteins like BAD [UniProt summary]. AKAP10 also regulates heme biosynthesis during erythropoiesis by directing PKA-mediated phosphorylation of ferrochelatase at the outer mitochondrial membrane 1. Clinically, AKAP10 polymorphisms significantly impact cardiovascular function. The common 646V variant (40% allele frequency) associates with increased basal heart rate and decreased heart rate variability—markers of reduced cholinergic sensitivity that predict sudden cardiac death risk 2. In healthy populations, the Val allele predicts higher resting heart rate and diminished heart rate variability 3. AKAP10 gene disruptions cause cardiac arrhythmias and premature death in mice 2, while specific polymorphisms are associated with reduced preterm birth risk in Malay populations 4 and elevated blood pressure in newborns 5. In oncology, elevated AKAP10 expression correlates with colorectal cancer progression, associating with tumor invasion depth, lymph node metastasis, advanced stage, and poor differentiation 67. AKAP10 also emerges as a dysregulated gene in primary sclerosing cholangitis, potentially mediating immune-driven disease mechanisms 8.