These findings position the Nrf2/NF-κB axis as a critical regulatory node in renal fibrosis and highlight a key question for future research: what is the precise molecular mechanism of the crosstalk—direct or indirect—through which Catalpol-mediated Nrf2 activation leads to the downstream inhibition of NF-κB? The gene discussed is NFKB1; the disease is renal fibrosis.