It is unlikely that the mutant ALOX12B genes with deletion of exon 3–15 can produce a protein with residual enzyme activity, thus we speculate that ALOX12B deficiency alone causes a mild, self-improving, ARCI phenotype, and that more severe ALOX12B-related phenotypes could depend on additional modifiers, genetic or epigenetic ones. Here, ALOX12B is linked to autosomal recessive congenital ichthyosis.