For example, in a passive smoking-induced lung injury model, it reduces lung tissue damage, apoptosis, and inflammatory responses by decreasing ATF6 activation while downregulating the expression of lung cancer-related genes (such as VEGF, CYP1A1, and CYP1B1) (119); in the Lewis lung cancer (LLC) mouse model, it significantly inhibits tumor growth by suppressing the NLRP3 inflammasome and ATF6-related pathways, accompanied by reduced expression of pro-angiogenic and lymphangiogenic markers in tumor tissues (120). The gene discussed is CYP1B1; the disease is neoplasm.