PTPA and Parkinson disease: PP2A was shown to modify Ser656, the same residue phosphorylated by PKA, and undo PKA‐mediated inhibition of Drp‐1 leading to mitochondrial fragmentation and depolarization.95 In neurons, PP2A activation of Drp‐1 led to decrease synapse formation and shorter and fewer dendrites.95 Excessive PP2A activity could be a player in neurological conditions that may have fragmented mitochondrial networks, such as PD.