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]. Here, RPS6KA3 is linked to colorectal cancer.