Molecular docking revealed that each bioactive compound (formononetin, cinnamaldehyde, gingerol, ursolic acid, anethole, and berberine) of HJT had favorable binding abilities with MYC, VEGFA, AKT1, JUN, MAPK3, CASP3, MAPK1, EGF, and TP53, further implying the potential molecular mechanism of action of HJT in GC. The gene discussed is AKT1; the disease is gastric cancer.