Of note, Apc/Min+ iTregs lost most of their inhibitory effect on tumor multiplicity yet they still retained a sizeable effect on inhibition of large tumors, suggesting that the defect in Apc/Min+ iTregs is mainly in controlling tumor induction while their inhibitory capacity to control tumor growth in tumor microenvironment is conserved similar to IL-17A KO Apc/Min+ Tregs. This evidence concerns the gene APC and neoplasm.