For instance, elevated KAL levels have been found in patients with type I and type II diabetes, and our recent study showed that elevated KAL can activate the NF-κB signaling pathway to cause chronic inflammation in diabetic wound tissues.13,14 Similarly, our present study shows that elevated KAL leads to NASH by down-regulating CGI58, reflecting a pro-inflammatory effect. This evidence concerns the gene NFKB1 and metabolic dysfunction-associated steatohepatitis.