Since the presence or absence of iBALT does not modify the course and severity of arthritis and heart disease development in BPSM1 mice, we suggest that it plays no part in these diseases, and that the extent of iBALT in chronic obstructive pulmonary disease and RA patients merely represents the severity of the inflammation in these patients, and possibly the amount of TNF produced in their lungs. This evidence concerns the gene TNF and rheumatoid arthritis.