Upon comparison with the panel of other pathogenic variants studied [12,13,17,19], it can be concluded that the loss/reduction in the ability to interact with RGS19 is a uniform feature of the GNAO1 encephalopathy mutants, regardless of whether they are deficient in GTP hydrolysis (as, e.g., G203R, E246K, or R209C) or not (as the P170R mutant studied here). The gene discussed is RGS19; the disease is Encephalopathy.