Malignant melanoma is the deadliest type of skin cancer due to its ability to evade all treatment attempts. It accounts for 75% of mortalities associated with skin cancer though it only constitutes 4% of total dermatological cancer incidences (Davis et al. 1367). CDC research statistics show that melanoma’s annual incidences and mortality rates have considerably increased in the last few decades. As of 2019, in every 100,000 people in the US, 22.1 are diagnosed with malignant melanoma (Davis et al. 1367). This dramatic increase in incidences can be attributed to modern-culture behaviors of sun-seeking and the migration of fair-skinned populations to regions near the equator (Davis et al. 1366). Given the high prevalence and mortality rates of melanoma, information about the risk factors and effects of this neoplasm is valuable in improving understanding of the disease. This essay reviews the causes of melanoma, including the genetic aberrations involved, and discusses some of the effects of this cancer. Melanoma arises from complex interactions between genetic and environmental factors. In the genetic aspect, the majority of the cases are due to inherited or acquired mutations in the MAP kinase pathway (Davis et al. 1368). MAPK contributes to carcinogenesis by disrupting the cell cycle and inhibiting apoptosis (Leonardi et al. 8). Epidemiological research implicates intense Ultraviolet radiation as the main cause of acquired mutations (Davis et al. 1368). This comes about due to intensive sun exposure and the acquisition of sunburns early in life (Liu and Sheikh 3). According to Davis et al., sunburns in childhood or early adolescence doubles the risk for melanoma in adult life (1367). Ultraviolet radiation increases the risk for skin cancers through DNA mutations, that is, by inducing the formation of pyrimidine dimers in DNA (Davis et al. 1367). Alternatively, UV rays facilitate tumorigenesis through the deamination of the cytosine base pair into thymidine. UV mutagenic effects are very potent to the point that the base pair alteration rate in malignant melanoma exceeds that of any other solid cancer. Malignant melanoma can also occur due to hereditary or familial mutations. According to Davis et al., 8-12% of patients with melanoma have a family history of this neoplasm (1368). Patients in this category are highly sensitive to UV rays, which are present in childhood. Importantly, malignant melanomas emanate from moles, and individuals from families with a history of melanoma develop numerous moles. Genetic profiling also shows there are different mutations in hereditary melanoma compared to the non-hereditary type. Approximately 40 % of familial melanoma shows a somatic mutation in the CDKN2A gene (Davis et al. 1369). This genetic aberration causes defects in tumor suppressor protein (P53) that regulate the G1-S checkpoint, causing uncontrolled cell proliferation. Hereditary melanomas develop earlier (average age 65 years) and present as multiple cancer lesions. Melanocytic nevi (benign lesions) predisposes patients to malignant melanoma. Nevi, colloquially known as birthmark or mole, are dark pigmentations on the skin composed of aggregates of