We demonstrated that a lack of CH25H leads to increased susceptibility to DSS-induced colitis, which may in part result from impaired epithelial compensation and regeneration mechanisms as indicated by the diminished expression of the mRNA levels of the tight junction genes ZO-1, ZO-2, Claudin-1, Claudin-2 and Claudin-3 in Ch25h-deficient mice compared with WT mice. The gene discussed is CLDN1; the disease is colitis.