The first and most obvious evidence of such crosstalk in melanoma microenvironment calls into play the upregulated tumor‐derived cathelicidin‐related antimicrobial peptide (CRAMP), the mouse analog of LL‐37 peptide in humans, by emphasizing its key role in reshaping tumor‐infiltrated FoxP3+ Th17 cells from effector Th17 cells into immunosuppressive Th17 cells via CD73 expression.77 This evidence concerns the gene CAMP and neoplasm.