Additionally, genetic deletion of RIPK1 in vivo triggered Z-conformation nucleic acid binding protein 1 (ZBP1)-dependent necroptosis and inflammatory activation, RIPK3-/- mice showed decreasing Colorectal cancer (CRC) via c-Jun N-terminal kinase (JNK) pathway and CXCL1 (C-X-C Motif Chemokine Ligand 1) pathways, and MLKL-/- mice were susceptible to DSS-colitis and AOM-DSS-CRC via MEK/ERK pathway [19]. This evidence concerns the gene CXCL1 and colitis.