The ability of CSPG4 to enhance ERK1/2 signalling is also amplified by the genomic landscape of patients with melanoma, as approximately 60% of human melanomas have been shown to express the constitutively active BRAFV600E mutant, which drives constitutive ERK1/2 phosphorylation and activation, likely by impacting growth factor-induced activation of Ras tyrosine kinases (RTKs). Here, CSPG4 is linked to melanoma.