Carriers of highly functional alleles of the UGT1A6 gene (19T>G, 552A>C, and 541A>G) demonstrated increased activity of the UGT1A6 enzyme compared to homozygous carriers of the wild-type allele, and carriers of the 552A>C SNV in the UGT1A6 gene had a longer half-life of toxic metabolites of VPA and a lower clearance rate, which often led to VPA-induced ADRs such as ataxia, liver damage, metabolic syndrome, tremors, hallucinations, pancreatitis, and weight gain. This evidence concerns the gene UGT1A6 and cerebellar ataxia.