In summary, Ephexin1 is upregulated by an oncogenic K-Ras mutant, and when phosphorylated at S16 and S18 by Akt, interacts directly with K-Ras, thereby activating the Raf/MEK/ERK signaling pathway and modulating the expression of K-Ras-mediated downstream target genes, which finally leads to increased tumor cell growth and proliferation (Fig. 6F). Here, AKT1 is linked to neoplasm.