Our observation that a CRISPR‐Cas9–mediated disruption of the MCAM gene in melanoma cells impairs their ability to migrate on endothelial cell surfaces in vitro and decreases their ability to develop spontaneous lung metastases in vivo functionally support the notion that MCAM mediates melanoma–endothelial interactions and thereby facilitates metastatic progression. This evidence concerns the gene MCAM and melanoma.