Our contribution can be summarized in two main key findings: (1) KMT2B, unlike KMT2A, is crucial for the MEF-to-iN conversion, both for the induction of transdifferentiation process per se and the maturation of the generated iNs; and (2) the molecular pathways underlying neuronal cell conversion, which we exposed through conditional ablation of Kmt2b, can illuminate the genetic basis of dystonia, a neurological disorder for which KMT2B mutations have been recently found as driving genetic leads.6,7. This evidence concerns the gene KMT2B and Dystonia.