CXCL1 and neoplasm: Mechanistic studies revealed that, on the one hand, RIP3 enhanced the proliferation of premalignant intestinal epithelial cells to facilitate the progression of CAC via activating JNK signaling; on the other hand, RIP3 promoted the myeloid cell-induced adaptive immune suppression to contribute to the CAC progression by CXCL1 signaling to increase the number of myeloid-derived suppressor cells and M2c-like macrophage tumor-associated macrophages while decreasing T-cell accumulation, infiltration and activation.