GNAO1 and Encephalopathy: 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).