After CNO (1 mg/kg) administration, ataxia-like behavioral analysis confirmed spiking inhibition in hM4Di-expressing CaMKIIα+ neurons in the FN of L7-Cre; BOD1f/f mice, accompanied by an increased latency time on the rotarod test, higher scores on the suspension test, decreased scores on the limb-clasping test and a shorter time spent on the pole in the pole test (Supplementary Fig. 6g–j). The gene discussed is CAMK2A; the disease is Ataxia.