In addition, signaling of the S6K enhances the level of the translation elongation factor eEF2 and leads to proteasomal degradation of the translation inhibitor programmed cell death 4 (PDCD4), which blocks RNA helicase activity of the eIF4A, required for unwinding highly structured 5′UTRs of cancer-promoting mRNAs [44,45]. This evidence concerns the gene RPS6KB1 and cancer.