Central pontine demyelination syndrome, or central pontine myelinolysis (CPM), is an uncommon but potentially devastating complication often seen in liver transplant recipients. Although classically associated with rapid correction of hyponatremia, an increasing body of evidence from case reports and small case-based series implicate calcineurin inhibitors such as tacrolimus as independent contributors to brainstem demyelination based on temporal association and improvement after drug withdrawal. Proposed mechanisms include endothelial dysfunction, blood–brain barrier disruption, and direct oligodendrocyte toxicity. MRI brain typically shows symmetric T2/T2-FLAIR hyperintensities in the pons.  Discontinuation of medication can lead to clinical and radiologic improvement, but outcomes are variable.