Autism spectrum disorders (ASD) are associated with defects in neuronal connectivity and are highly heritable. Genetic findings suggest that there is an overrepresentation of chromatin regulatory genes among the genes associated with ASD. ASH1 like histone lysine methyltransferase (ASH1L) is a chromatin regulator that was identified as a major risk factor for ASD. However, how mutations in ASH1L lead to deficits in neuronal connectivity associated with ASD pathogenesis is not known. In their new study titled "Counteracting epigenetic mechanisms regulate the structural development of neuronal circuitry in human neurons", members of the Lizarraga lab reveal  that ASH1L regulates neuronal morphogenesis by epigenetically modulating pathways like the BDNF-TrkB signaling pathway. This work was led by Sunny Cheon, a former technician in the Lizarraga lab, and Allie Culver, a graduate student co-mentored by Drs. Lizarraga and Davis. In addition, graduate students Foster Ritchie, Janay Vacharasin and Trevor Moreland, former undergraduate students Anna Bagnell, Mikayla McCord, Austin J. Smith, Mara Cowen, and collaborators Shannon Davis, as well as Carin Papendorp & Judy Liu from Brown University contributed to this work. Congrats!