Free fatty acid-induced steatosis was relieved and nonalcoholic steatohepatitis (NASH)-related mechanisms were inhibited in HepG2 cells treated with 30% ethanolic extract of A. capillaris, including activation of c-Jun NH2 terminal kinase (JNK) and p53-upregulated modulator of apoptosis (PUMA) [34]. Here, BBC3 is linked to metabolic dysfunction-associated steatohepatitis.