Rheumatoid arthritis (RA) is one kind of chronic inflammation disease. It affects not only joint, but often has the infringement outside the joint, such as internal organs. Besides the environmental factor, the heredity factor is involved in the pathogenesis of RA too. HLA-DR4 was found to play a role in RA pathogenesis in Taiwan. Because the DR4 positive patients actually are only one-half, other than HLA-DR gene may also be involved in RA pathogenesis. NF£eB plays an important role in immune inflammation. Activity of I£eB can affect NF£eB. I£eB£\ is a critical member in the I£eB protein family. Moreover, I£eBL is functionally similar to I£eB£\. Therefore we extrapolated polymorphisms of I£eBL gene and I£eB£\ gene of the RA patients and normal subjects. In this research, studies of these two genes from 79 RA patients and 81 normal subjects were divides into two parts. The first part used polymerase chain reaction, direct sequencing, special sequence polymerase chain reaction as well as limit fragment length polymorphism to study relations between I£eBL gene and HLA-DR4 and RA occurrence. The second part used polymerase chain reaction and limit fragment length polymorphism, to analyze relation between I£eB£\ gene and the RA occurrence. We found that there is significant increase of -421 -/A base deletion polymorphism in I£eBL gene from DR4 positive RA patients and -262 T/C polymorphism in I£eBL gene from DR4 negative RA patients. A significant reduction of -519 C/T polymorphism in I£eB£\ gene from DR4 negative RA patients was found too. In conclusion, polymorphisms of -421 -/A base deletion as well as -262 T/C in I£eBL gene may be involved in the pathogenesis of RA by alteration of I£eBL activity and thereafter binding of I£eBL to NF£eB.