This finding extends the canonical apoptosis paradigm: although elevated Bcl-2/Bax ratio as an apoptotic hallmark exhibits cross-species conservation—validated in vertebrate models (hepatic fibrosis [31], environmental toxin-induced grass carp hepatotoxicity [32], human thyrocyte dysfunction [33]) and invertebrate systems (marine rotifer stress response [34])—our work delineates its pathogen-triggered molecular axis. This evidence concerns the gene BCL2 and Hepatic fibrosis.