We have recently discovered a profound upregulation (mean 204 fold) of the microRNA (miRNA) miR-514a-3p in 38/55 (69%) cutaneous melanoma cell lines compared to several other cancer types (3% or 1/34). This miRNA is a member of a cluster (miRNA-506-514) that has been shown previously to be involved in initiating melanocyte transformation along with promotion of melanoma growth. We have shown that miR-514a-3p specifically targets NF1, a tumour suppressor in melanoma. Generally, miRNAs negatively regulate target genes by binding to the transcript’s 3’UTR however in this instance the NF1 mRNA has miR-514a-3p specific binding sites in its coding sequence (exons 9 and 23). Using a Dual-Luciferase Reporter assay, and following site-directed mutagenesis, we have shown a 4-5 fold recovery of luciferase signal compared to endogenous levels when both binding sites were mutated. NF1 negatively regulates H/KRAS and NF1 inactivation has been implicated in resistance to RAF/MEK-targeted therapies. Large-scale genome and exome sequencing projects have shown that NF1 loss of function can be frequently attributed to truncating mutations. Alternatively, we propose that binding of miR-514a-3p to NF1 transcripts provides another mechanism for the dysregulation of the MAPK pathway which may account for resistance to current therapies.