Dephosphorylation of AKAP‐1 can lead to its ubiquitination by E3‐ubiquitin ligase seven in absentia 2 (Siah2) resulting in its degradation.244 This ultimately diminishes PKA concentrations on mitochondria, which can impair the beneficial effects of local PKA signaling.244 Given the anomalies related to PKA signaling in neurodegenerative disorders, it is likely that disorientation and destabilization of AKAP‐1 on the OMM could be responsible for the lack of mitochondrial health in conditions such as AD and PD. The gene discussed is AKAP1; the disease is Alzheimer disease.