Melanoma is ideal to study non-tumor cell-autonomous metastasis-suppressor roles for SSeCKS because, unlike many other cancers [19], SSeCKS/AKAP12 expression is not super-downregulated in human melanoma metastases compared to primary-site lesions (Figure 1A), and the loss of AKAP12 expression does not alter melanoma survival (Supplementary Figure 1A). Here, AKAP12 is linked to melanoma.