Therefore, our data uncover an interaction between the two pathways affecting YB-1 activity and, under this condition, dual targeting of PI3K and MEK becomes an efficient approach to block proliferation as depicted in Figure 5C. According to this model, RSK targeting cannot be used as an effective approach to target YB-1, a conclusion that is also supported by the study in colorectal cancer cells using RSK inhibitor LJI308 [52]. The gene discussed is RPS6KA1; the disease is colorectal cancer.