Furthermore, Koppe et al. demonstrated that RIPK1 is the main players of the NF-κΒ-independent IKKα/βLPC-KO phenotype of mice characterized by cholestasis, reduced compensatory proliferation and then carcinogenesis, underlying a role of the catalytic IKKs in controlling RIPK1 activity independently of NF-κΒ (Fig. 4b)137. This evidence concerns the gene RIPK1 and cholestasis.