According to these studies, the silencing of S6K2 was able to decrease the cell viability of small-cell lung cancer (SCLC) cells, as well as non-small-cell lung cancer (NSCLC) cells, either via preventing the formation of the FGF2-inducible PKCε/B-RAF/S6K2-complex or the downregulation of the Hedgehog/GLI pathway, respectively [12,13]. This evidence concerns the gene PRKCE and non-small cell lung carcinoma.