In fact, intestinal epithelial-specific Slco2a1-deficient mice has lower susceptibility to experimental colitis as with the model in the study by Zhang et al. Although suppressed PGE2 metabolism in macrophages might contribute to the enhanced PGE2 concentration, Slco2a1ΔMP only partially reproduced the systemic knockout phenotype in the present study. Here, SLCO2A1 is linked to colitis.