Figure 8. Schematic model of this study. After the combination treatment of lonafarnib and sorafenib, ATG3 protein was increased and facilitated the conversion of LC3-I to LC3-II, which activates the autophagic flux that recruits cyclin D1 protein into autolysosome and promotes its degradation. The lack of cyclin D1 leads to hypophosphorylation of Rb protein, and subsequent inhibition of DNA synthesis.