The largest organ with immune function, the skin, has complex structure and various physiological functions. Cells comprising this complex structure sustain various processes and have proteomic/transcriptomic/genomic patterns that would subside to developing a specific function in a specific moment of time and in a defined space. Within the complex skin structure melanocyte is one of the cell types that is involved in skin’s main functions. In the process of normal melanocyte transformation into a neoplastic cell there are several stages that are favored by a protumor inflammatory milieu. A tumorigenesis-friendly environment would increase cell’s genetic instability that will further lead to tumorigenesis and additionally to metastasis. In the environment, immune cells and immune-related molecules seminally contribute to the inflammatory landscape. Melanomagenesis is not a straight forward process. In order to take place, various factors need to collide, environmental, genetic, and immune factors must conjoint. Melanomas are heterogeneous and the transformed melanocyte has various genetic alterations, these mutations being specific to the site, to the degree of UV exposure, and/or specific for the genetic make-up of the host’s organism. This variability suggests that melanoma has more than one causal pathway. Within our paper we will snapshot the cellular identity of normal melanocyte, through benign transformed melanocyte up to a full blown tumorigenesis. Factors that are triggering these transformations(s) will be briefly highlighted.