Additionally, the network pharmacology and protein phosphorylation chip technology indicated that THY-10A62 effectively reduced the phosphorylation level of FAK protein and concurrently modulated the phosphorylation levels of downstream effectors RASGRF1 and BRAF in the FAK signaling pathway (Figure 5, Supplementary Figure 3, Supplementary Table 9), representing a potential regulatory mechanism by which THY-10A62 suppresses liver cancer cell proliferation. This evidence concerns the gene RASGRF1 and liver cancer.