Our data allowed us to hypothesize that such ACE-binding protein is chemokine CCL18 and ACE phenotype in the S13 patient (which is similar to the phenotype of ACE in Gaucher spleen) could be explained by binding of the excess of CCL18 (due to Niemann–Pick disease phenotype in this patient) to ACE in the S13 patient, which prevents anti-catalytic action of albumin towards ACE. This evidence concerns the gene ACE and Niemann-Pick disease.