When comparing treatment-naïve and dabrafenib- or vemurafenib-treated melanoma patients, several studies have identified PI3K-AKT activation downstream of the platelet-derived growth factor receptor β (PDGFRβ) or the insulin-like growth factor 1 receptor (IGF1R) as a mechanism of therapy resistance [11,12,13]. This evidence concerns the gene IGF1R and melanoma.