This trend in the structural rearrangements likely reflects the mechanism behind the ability of Zn2+ to recover the GTPase reaction of the three pathologic mutants, their cellular interactions with RGS19 and AGS3, and ultimately provide motor activity and longevity ameliorations in the Drosophila model of GNAO1 encephalopathy upon dietary zinc supplementation. The gene discussed is RGS19; the disease is Encephalopathy.