ATP2A1 and Brody myopathy: Protein analyses showed near absence of SERCA1 and a significant twofold increase in SERCA2 content in affected muscle that was confirmed by immunofluorescent confocal microscopy showing SERCA2 upregulation in both slow- and fast-twitch fibers, providing the first clear evidence of a compensatory mechanism that partially restores diminished Ca2+ transport in Brody myopathy.