The data presented in this work show the long lasting effect of mildly increased maternal corticosterone during lactation on TNBS colitis in three-month old male rats, and take into account the variations in some indices of the pathology (histological score, colonic MPO activity, body weight and food intake) and the involvement of the main peripheral endogenous systems: mast cells, glucocorticoids (GCs) and their receptors (GRs), corticotrophin releasing factor (CRF) and its receptor, CRH-1R, known to be involved in the onset and progression of colitis [10], [28]–[33]. This evidence concerns the gene BCL2A1 and colitis.