NFKB1 and rheumatoid arthritis: Under M1-polarizing conditions, 65–79*SE upregulated the expression levels of many genes that are known to code for pro-inflammatory or known RA disease markers, as well as genes coding for confirmed—or proposed—therapeutic targets, and pathogenic mechanisms, such as osteoclastogenesis, NF-κB activation, angiogenesis, or M1 polarization.