Considering earlier findings and recognizing the crucial role of comprehending the mechanisms behind NF-κB pro-inflammatory functions to improve therapeutic approaches for inflammation-related diseases, we investigated the gene expression and the protein expression level of p65 iso5 in the PBMCs of FD patients with classic and late-onset phenotypes, as well as with GVUS mutations. This evidence concerns the gene NFKB1 and Fabry disease.