The results indicate that FFBZL may effectively bind to apoptotic targets through its active components; downregulate the expression of the key apoptosis targets GSK3B, PIK3CA, FN1, MET, SPP1, and MAPK3; and regulate the PI3K-Akt pathway, promoting tumor cell apoptosis to exert antitumor effects and thereby improving the prognosis of OSCC patients (Figure 9). This evidence concerns the gene AKT1 and neoplasm.