GNAL encodes Gαolf, a stimulatory G protein alpha subunit enriched in the striatum and olfactory neuroepithelium that functions as a transducer in G protein-coupled receptor (GPCR) signaling. GNAL contains a guanine nucleotide binding site and cycles between inactive GDP-bound and active GTP-bound states 1. Upon GPCR activation, GNAL promotes GDP release and GTP binding, subsequently activating adenylyl cyclase 3 (ADCY3) to increase cAMP levels, with GTP hydrolysis terminating the signal 1. In the striatum, GNAL specifically mediates dopamine D1 and adenosine A2A receptor signaling through the AC-cAMP cascade. Loss-of-function GNAL mutations cause DYT-GNAL dystonia (Dystonia 25), an isolated focal and/or segmental dystonia with adult-onset presentation and preference for upper-body involvement 2. GNAL mutations account for approximately 1.1% of dystonia cases in literature 3. The pathophysiology involves profound alterations in striatal dopamine receptor signaling; heterozygous GNAL loss reduces adenylyl cyclase AC5 expression, impairs D2 receptor-mediated inhibitory responses in cholinergic interneurons, and disrupts normal corticostriatal plasticity 1. Tremor occurs as an additional phenotypic feature in some DYT-GNAL patients 4. GNAL-related dystonia reflects dysfunction within the basal ganglia-sensorimotor network 5.