Although the corticospinal tract and connectivity in the mouse are different from that of the human, previous studies using a spontaneous mutation allele that removes the exon encoding the P3 intracellular domain of DCC have shown that homozygous Dcckanga/kanga and Dcckanga/− mice exhibit a hopping gait, ataxia, and abnormal pyramidal decussation through adulthood, thus recapitulating to some extent the motor phenotype of DCC haploinsufficient individuals (Finger et al., 2002; Welniarz et al., 2017). This evidence concerns the gene DCC and cerebellar ataxia.