One study analysis confirmed that tumor necrosis factor gene expression was higher in FD patients than in controls, and it was also hypothesized that there is a feed-forward loop between tumor necrosis factor, Gb3, and FD-induced pain, in which tumor necrosis factor further stimulates Gb3 loading of neurons and alters the expression of pain-associated ion channels, thus contributing to the analgesic effect. This evidence concerns the gene TNF and Fabry disease.