It is tempting to speculate that if nervous and immune system cells of ABCD1 mutation carriers indeed have aberrant PEX11B and ULK1 activity, this could lead to differences in peroxisome abundance and/or activity that increase reactive oxygen species (ROS) levels and promote X-ALD pathogenesis. The gene discussed is PEX11B; the disease is X-linked adrenoleukodystrophy.