Inappropriately low mobilization of AMPK signaling did however provide an explanation for several features of RA T cells: reduced mitochondrial activity and reduced ATP synthesis; low intracellular ROS concentrations; shunting of glucose into the PPP instead of into pyruvate generation; inability to metabolize surplus lipids, and persistently high activation of mTORC1. Here, PRKAB1 is linked to rheumatoid arthritis.