Here, we found M-CSF and TGFβ secreted from SK-MEL-28-RhS to also play a role in the SK-MEL-28-RhS-mediated immune modulation, which might explain why IL-10 blockade alone was not sufficient to reverse the melanoma-induced conversion of monocyte into M2-like cells [15]. This evidence concerns the gene CSF1 and melanoma.