Melanoma, a highly lethal skin cancer, continues to pose significant challenges in treatment due to its metastatic spread and recurrence. Recent research has highlighted the interplay between immune escape and metastasis, challenging the traditional view of these processes as separate phenomena. The article discusses how mechanisms such as epithelial-to-mesenchymal transition (EMT), neural crest stem cell (NCSC) gene involvement, and hypoxia/acidosis are simultaneously involved in both immune escape and metastasis. EMT, a process that allows cells to lose epithelial characteristics and gain mesenchymal properties, is linked to both immune evasion and metastasis. NCSC genes, which are crucial for neural crest development, can be repurposed by melanoma cells to enhance their metastatic and immunosuppressive capabilities. Hypoxia and acidosis, common features of melanoma, create an environment that promotes EMT, metastasis, and immune escape. The article also explores the role of specific genes and pathways, such as SHC4, BRN3A, SATB2, LPAR1, NCAM, BMPs, and AQP-1, in driving these processes. Additionally, it discusses the reversible nature of melanoma progression under normal conditions, suggesting potential therapeutic opportunities. The article concludes by emphasizing the need for further research to understand the complex mechanisms underlying immune escape and metastasis in melanoma, which could lead to more effective treatments.Melanoma, a highly lethal skin cancer, continues to pose significant challenges in treatment due to its metastatic spread and recurrence. Recent research has highlighted the interplay between immune escape and metastasis, challenging the traditional view of these processes as separate phenomena. The article discusses how mechanisms such as epithelial-to-mesenchymal transition (EMT), neural crest stem cell (NCSC) gene involvement, and hypoxia/acidosis are simultaneously involved in both immune escape and metastasis. EMT, a process that allows cells to lose epithelial characteristics and gain mesenchymal properties, is linked to both immune evasion and metastasis. NCSC genes, which are crucial for neural crest development, can be repurposed by melanoma cells to enhance their metastatic and immunosuppressive capabilities. Hypoxia and acidosis, common features of melanoma, create an environment that promotes EMT, metastasis, and immune escape. The article also explores the role of specific genes and pathways, such as SHC4, BRN3A, SATB2, LPAR1, NCAM, BMPs, and AQP-1, in driving these processes. Additionally, it discusses the reversible nature of melanoma progression under normal conditions, suggesting potential therapeutic opportunities. The article concludes by emphasizing the need for further research to understand the complex mechanisms underlying immune escape and metastasis in melanoma, which could lead to more effective treatments.