In M2-polarizing conditions (Fig. 7F), a pro-M1 and pro-angiogenic upstream regulator Irf3, and the pro-M1 pro-arthritis upstream regulator Irf7, and NF-κB were all predicted to be activated by 65–79*SE, and reciprocally inhibited by 65–79*PE. Here, IRF3 is linked to arthritic joint disease.