To disentangle the effect of the different p62-regulated pathways and to circumvent the premature lethality of ubiquitous p62 ablation in the context of NEMO-dependent CLD, we generated NEMOLPC-KO mice with LPC-specific or whole-body expression of p62ΔEx2-5 (NEMOLPC-KO p62ΔEx2-5LPC and NEMOLPC-KO p62ΔEx2-5, respectively; Figure 4A). This evidence concerns the gene IKBKG and congenital secretory chloride diarrhea 1.