Carriers of UGT1A6 19T>G, 552A>C and 541A>G alleles displayed increased UGT enzyme activity than the wild-type patients, and UGT1A6 552A>C carriers showed a longer elimination half-life and a lower clearance rate frequently causing VPA-related ADRs, such as ataxia, liver damage, metabolic changes, tremor, hallucinations, pancreatitis, and weight gain [80,81]. This evidence concerns the gene UGT1A6 and cerebellar ataxia.