It is worth to notice that, regarding the CK2/BRAF nexus, a study demonstrated that the knock-down of CK2 in BRAF mutant melanoma cells was indeed accompanied by increased sensitivity to RAF-MEK inhibitors (with downstream effect on ERK phosphorylation); however, the authors proposed a kinase-independent scaffolding function of CK2, since the resistance to RAF-MEK inhibitors was promoted by overexpression of a CK2 kinase-inactive mutant [90]. This evidence concerns the gene BRAF and melanoma.