This review discusses immune escape and metastasis mechanisms in melanoma, highlighting their interconnected nature. Melanoma, a highly aggressive skin cancer, has seen limited success with current therapies, particularly in resistant cases. Melanoma cells employ various strategies to evade the immune system and metastasize to distant organs. Recent research suggests that tumor cells can disseminate early during melanoma progression and enter dormant states, leading to future metastases. Immune escape and metastasis were previously viewed as separate phenomena, but accumulating evidence indicates they are closely linked. Mechanisms such as epithelial-to-mesenchymal transition (EMT), neural crest stem cell genes, and hypoxia/acidosis are involved in both processes. Understanding these mechanisms can lead to novel strategies to combat melanoma progression. The review also explores immune escape mechanisms, including defective immune recognition and immune checkpoint receptors, and their roles in melanoma progression. EMT is linked to immune escape and metastasis, with EMT-TFs playing a key role. Neural crest stem cell genes are also involved in EMT and metastasis. Hypoxia and acidosis contribute to immune escape and metastasis by creating an immunosuppressive environment. Recent studies show that melanoma cells can enter a dormant state, which may lead to metastasis later. The review emphasizes the importance of understanding these mechanisms to develop effective treatments for melanoma.This review discusses immune escape and metastasis mechanisms in melanoma, highlighting their interconnected nature. Melanoma, a highly aggressive skin cancer, has seen limited success with current therapies, particularly in resistant cases. Melanoma cells employ various strategies to evade the immune system and metastasize to distant organs. Recent research suggests that tumor cells can disseminate early during melanoma progression and enter dormant states, leading to future metastases. Immune escape and metastasis were previously viewed as separate phenomena, but accumulating evidence indicates they are closely linked. Mechanisms such as epithelial-to-mesenchymal transition (EMT), neural crest stem cell genes, and hypoxia/acidosis are involved in both processes. Understanding these mechanisms can lead to novel strategies to combat melanoma progression. The review also explores immune escape mechanisms, including defective immune recognition and immune checkpoint receptors, and their roles in melanoma progression. EMT is linked to immune escape and metastasis, with EMT-TFs playing a key role. Neural crest stem cell genes are also involved in EMT and metastasis. Hypoxia and acidosis contribute to immune escape and metastasis by creating an immunosuppressive environment. Recent studies show that melanoma cells can enter a dormant state, which may lead to metastasis later. The review emphasizes the importance of understanding these mechanisms to develop effective treatments for melanoma.