Homozygotes are viable, fertile, and appear normal in growth and morphology. The liver and hepatocytes are normal. No hepatic fatty metamorphosis nor spontaneous peroxisome proliferation is seen in these mutant mice, as occurs in mice deficient for Acox1 (Acox1^tm1Jkr). Acox1 is the first enzyme in the classical pathway of peroxisomal beta-oxidation of fatty acids. The constitutive and induced levels of other fatty-acid metabolizing enzymes do not appear to be affected in mutants. In wild-type mice, ciprofibrate and Wy-14,643 induce peroxisome proliferation; this reaction, however, is blunted in Ehhadh^tm1Jkr mutants (J:55395).