CSF2 and melanoma: In agreement with that, we find expression of GM-CSF also in the stromal fibroblasts of perilesional skin and in the microenvironment of cSCC from vemurafenib-treated melanoma patients, suggesting that the fibroblast-derived GM-CSF supports keratinocyte differentiation also in situ. Therefore, we hypothesize that vemurafenib-dependent upregulation of GM-CSF is a further activity contributing to the formation of hyperkeratotic lesions and well-differentiated KAs and cSCCs in the melanoma patients (40–42).