Studies have demonstrated that down-regulation of LOXL1 can slow disease progression (44), and HSC-specific LOXL1 knockout in a mouse model of non-obese NASH attenuated liver steatosis, inflammation, and fibrosis, suggesting that LOXL1 may be involved in HSC activation and fibrogenesis (45). Here, LOXL1 is linked to metabolic dysfunction-associated steatohepatitis.