The most likely candidate for mediating the residual β-oxidation activity (29%) for C26∶0 in the Abcd1/Abcd2 double-deficient MPMΦ is the third peroxisomal ABC transporter, ABCD3, in similarity to human X-ALD fibroblasts [7] and monocytes [41]. Here, ABCD1 is linked to X-linked adrenoleukodystrophy.