Given that our MPRA assay was conducted in melanoma cells, it may be possible that such variants, for example, may only be functioning in the context of oncogenic signaling (e.g., oncogenic BRAF), tumor suppressor loss (e.g., CDKN2A), or immortalizing events (e.g., mutation of the TERT promoter). Here, CDKN2A is linked to neoplasm.