While our previous data indicated that abrogated LIGHT–LTβR interactions are responsible for severe disease,6,10 a previous study found that the absence of LIGHT was protective38 and that the absence of LTβ was the relevant ligand for increased colitis when it was missing from T cells.35 Although the previous work analyzed an acute DSS-induced model, in our experiments, deficiency for LIGHT accelerated disease in both the acute and chronic models.6 Likely this discrepancy may be due to microflora or other differences in mouse colonies. This evidence concerns the gene TNFSF14 and colitis.