CRISPR/Cas9 technology generated a CA-to-G change resulting in a frameshift and immediate premature stop codon in place of methionine codon 533 (p.M533*fs*1). This corresponds to the human chr4:49034669CA>C:p.L533*fs* mutation associated with idiopathic normal pressure hydrocephalus (iNPH). Immunohistochemistry shows loss of expression in the ventricular epithelia of homozygous mice.