Indeed, having confirmed that the bgm allele used by Min and Benzer (1999) is a null, we show here that a far more profound phenotype, and thus a better ALD disease model, is found in double-mutant animals harboring mutations not only in the bgm-encoded ACSL, but also in its homolog, the double bubble (dbb)-encoded ACSL. This evidence concerns the gene ACSBG1 and adrenoleukodystrophy.