Tregs impair tumor rejection by suppressing the cytotoxicity of tumor-specific CD8+ T cells.46 Consequently, Treg depletion leads to intratumoral accumulation of activated cytotoxic CD8+ T cells and tumor regression.19 In AOM/DSS-treated mice, these cytotoxic CD8+ T cells directly control CRC development.19 Although ST2 expression has been associated with an activated phenotype and an improved capacity of Tregs to restrain T cell proliferation in vitro,41 we did not detect difference in the suppressive function of ST2+ versus ST2− Tregs in our model. The gene discussed is IL1RL1; the disease is neoplasm.