We surprisingly found that the deletion of Atg16l1 led to a significantly increased tumor prevalence in Atg16l1/Xbp1/Rnaseh2bΔIEC mice (no functional autophagy present to compensate for defective UPR) compared to Xbp1/Rnaseh2bΔIEC mice (autophagy compensates for the defective UPR) of the same age. The gene discussed is ATG16L1; the disease is neoplasm.