Similarly, while genetic defects in CPT1 and CPT2 have been shown to underlie pathogenic responses to VAs, including rhabdomyolysis, hyperkalemia, metabolic acidosis, and even acute renal failure and cardiac arrest (Benca and Hogan, 2009; Wieser et al., 2008; Cornelio et al., 1980), the role of CPT1 has not been directly probed in relation to anesthesia in normal patients or in genetic mitochondrial disease. Here, CPT2 is linked to metabolic process.