The protein interaction models build reference to the human disease complex of hereditary spastic paraplegias (HSPs) and possibly Parkinson's disease (Jaberi et al., 2016), rather than to multiple sclerosis, in addition to primary torsion dystonia by interaction to GNAL (Fuchs et al., 2013) and to severe hypotonia by GNB1 (Petrovski et al., 2016). Here, GNAL is linked to early-onset generalized limb-onset dystonia.