STX17 and metabolic dysfunction-associated steatohepatitis: Conversely, enhancing autophagy through mechanisms such as the overexpression of PLAC8 can improve AT2 cell survival and mitigate fibrosis.[19] Previous work demonstrated that Hcy induced the homocysteinylation (Hcy‐lation) and ubiquitination of Syntaxin 17 (STX17), a key autophagosome/lysosome fusion protein, in NASH, leading to an autophagy blockade and promoting fibrosis.[13] However, whether Hcy‐mediated modification of STX17 occurs in IPF, and its potential role in disease pathogenesis, remains unknown and warrants further investigation.