Scheeren et al. have found a cell-intrinsic role for Toll-like receptor 2 (TLR2) in tumorigenesis. They found that ablation of Tlr2 or myeloid differentiation primary response gene 88 (Myd88; which functions downstream of TLR2) reduced inflammation-induced tumorigenesis of intestinal epithelium. Furthermore, deletion of Tlr2 and Myd88 in mammary epithelium reduced the mammary repopulating unit frequency, and TLR2 inhibition reduced the growth of human breast cancers.