During the generation of a line of mice with knockout of the gene Park7 we noted an early movement disorder that was inherited independently of targeting vector transmission. Our initial observations suggested the affected mice suffered from an apparently paroxysmal movement disorder, often induced by touch. The abnormal movements occurred predominantly below the cervical level, and the disorder appeared progressive. At initial examination, a human movement disorder specialist (K. G.-H.) likened the disorder to episodic intermittent ataxia or kinesiogenic paroxysmal dystonia and predicted the involvement of an ion channel mutation in the etiology. Affected mice presented at approximately postnatal day 14, and survival time without weaning was on average 4 wk after onset.