Some examples are as follows: knockdown of the ST6Gal1 gene or the use of sialyltransferase inhibitors negatively impacts the efficiency of somatic cell reprogramming [191], failure to synthesize the GM3 induced by a homozygous loss-of-function mutation in the gene encoding GM3 synthase (ST3Gal5) results in infantile-onset symptomatic epilepsy syndrome [192], while mutations in the human ST8SIA1 gene are associated with an increased risk of developing multiple sclerosis [193]. This evidence concerns the gene ST3GAL5 and multiple sclerosis.