Our data suggest that the inhibition of different mechanisms, such as factors involved in the ER stress response (CHOP, BiP and caspase-12), UPR signaling branches (ATF6, ATF4, XBP-1s), the mitogen-activated protein kinase JNK, Bcl-2 family proteins, and caspase activation, would be implicated in the beneficial effects of glutamine in experimental colitis. The gene discussed is BCL2; the disease is colitis.