Conversely, 65–79*PE was predicted to activate key M2-inducing and anti-arthritis transcription factors Stat6 and Klf2, and inhibit pro-arthritis (Irf5, Irf7), pro-osteoclastogenic (Nfatc2, Ezh2), pro-angiogenic (Nfatc2, Ezh2, Gata6, Klf6, Irf3), pro-inflammatory (Irf5, Klf6), and pro-M1 (Klf6, Irf3, Irf7) upstream regulators (Fig. 7E). This evidence concerns the gene NFATC2 and arthritic joint disease.