As hepcidin, which reflects human macrophage-Mtb pathogen interactions through the regulation of iron metabolism and inflammation and for which we have reported a high performance to distinguish TB disease from pneumonia of other causes, the differential expression of SULT4A1 and WASPF via the sulfonation of Mtb products, the regulation of the actin cytoskeleton in the macrophages, may also be due to human macrophages-Mtb interactions contributing to host defense. The gene discussed is SULT4A1; the disease is susceptibility to pneumonia measurement.