In addition to tumor mutations that affect cell proliferation and survival largely via constitutive activation of the MAPK [15] and the phosphoinositide 3-kinases (PI3K) [16] pathways, as well as inhibition of tumor suppressors, such as phosphatase and tensin homolog (PTEN) [17], which impairs PI3K signaling [18], mechanisms that promote tumor invasion and infiltration are of particular importance in melanoma [19]. Here, PTEN is linked to melanoma.