CRISPR-Cas9 technology was used to introduce a one-nucleotide duplication in exon 4, inducing a translational frameshift expected to lead to the complete absence of encoded protein or the production of a truncated protein. RT-PCR analysis of testis mRNA revealed that the level of mRNA amplification was significantly reduced in homozygous mutant mice. Sanger sequencing of mRNA confirmed the production of abnormal transcripts with a premature stop codon 12 nucleotides after the first modified codon at position 135. (J:279937)