Furthermore, C4BPA and IL-26 are immune-related complement system genes and inflammation-related factors, respectively, and it has been suggested that the deletion of exon 2 of ABCD1 could affect the nonspecific complement system or immune-inflammatory system due to demyelination of neurons (Gupta et al., 2021) or metabolic disorder of immune factors (Swaminathan et al., 2022) in some patients with ALD. This evidence concerns the gene C4BPA and metabolic disease.