Our findings provided pharmacological evidence supporting the potential of DC32 in RA therapy and illuminated the mechanisms of Nrf2/HO-1 activation: DC32 increased the transcription and nuclear translocation of Nrf2 and then facilitated the transcription of p62, which magnified the activation of Nrf2/HO-1 by an autophagy-dependent Nrf2-p62-Keap1 feedback loop (51). The gene discussed is HMOX1; the disease is rheumatoid arthritis.