The exact pathophysiology of CNI‐induced neurotoxicity, including PRES, is unclear but seems multifactorial.35, 36 Impairment of oxidative phosphorylation by CNIs and thereby mitochondrial dysfunction has been reported to be a possible cause.37, 38 Mitochondrial dysfunction plays an important role in the pathophysiology of MMA, and FGF‐21 is a biomarker for mitochondrial dysfunction. This evidence concerns the gene FGF21 and Posterior Leukoencephalopathy Syndrome.