Using CRISPR-Cas9 gene editing technology, we engineered a variant of the B16-F1 murine melanoma cell line that carries a bi-allelic disruption in the Foxc2 gene and that does not express FOXC2 protein, and we reported that this B16-F1ΔFOXC2 variant grows out with slower kinetics as a subcutaneous tumor than its parental counterpart. This evidence concerns the gene FOXC2 and neoplasm.