For instance, the continuous presence of the TLR4 ligand LPS may result in a state of ER hyporesponsiveness by suppressing the proapoptotic C/EBP homologous transcription factor (CHOP),117 thus decreasing cellular sensitivity to cytotoxic stress, e.g., in DSS-induced acute colitis, as outlined above.118 On the other hand, deficiency in TLR4 may reciprocally promote conditions of direct or indirect ER stress119 which may contribute to aggravation of colitis. Here, TLR4 is linked to colitis.