Using the CPC-APC mouse model (mice that have Apc allelic loss specifically in the colonic epithelium and develop tumors primarily in the distal colon), Grivennikov et al. recently showed that microbial products, such as LPS, could activate interleukin 23 (IL-23) in tumor-associated myeloid cells and, subsequently, interleukin 17A (IL-17A) to drive tumor growth and progression (Grivennikov et al., 2012). Here, APC is linked to neoplasm.