Because NF-κB is a critical transcription factor that regulates the expression of cytokine genes and our data showed that EA suppressed the TNBS-induced NF-κB in the colon, we speculated that EA at PC3 and PC6 inhibited the expression of TNBS-induced cytokines via the suppression of NF-κB and affected immunity and inflammatory pathways, leading to the improvement of TNBS-induced colitis (Figure 4). Here, NFKB1 is linked to colitis.