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Cutaneous melanoma incidence increases with age, although it also affects young patients. The most important risk factor for melanoma is naevus counts, which also shows an age-related pattern of onset and disappearance, with naevi usually decreasing in number after 35-40 years of age. Decreased naevus counts has been associated with markers of biological ageing such as decreased bone mineral density and reduced cognitive function. Interestingly, both melanoma and high naevus counts have been associated in several studies with increased telomere length, another important biomarker of biological age. Similarly, an intriguing positive association between melanoma risk and history of acne has also been recently proposed, with history of acne showing an association with increased telomere length. Taken together, this evidence suggests that an inverse relationship exists between biological age and melanoma risk. Late-onset melanoma has specific characteristics which set it apart from its early-onset form, including higher Breslow thickness and higher mitotic rate, which contribute to more dire prognosis. Skin ageing is likely to play a role in melanoma, and it is regulated by intrinsic mechanisms, including decreased lipid production, likely involved in a greater susceptibility of the skin to damage and disease; as well as extrinsic causes, such as sun exposure, which is also responsible for accelerated skin ageing and is a well-known melanoma risk factor. In this thesis, I present the analyses I have conducted during my PhD to investigate the relationship between melanoma and age. I began my investigations by analysing markers of biological age, i.e., acne history and naevus counts, and their regulation at the genetic and transcriptomic level. Then, I explored intrinsic and extrinsic factors involved in skin ageing. Firstly, I examined intrinsic causes by studying the age-related changes undergone by sebum lipids and by skin gene expression levels. Then, I moved towards extrinsic causes and explored the genetic mechanisms regulating sun-seeking behaviour. Through my research, I have identified a connection between acne history and the p53 signalling pathway, which may explain the link between acne and melanoma susceptibility. Then, by participating in a large Genome-wide association study (GWAS) meta-analysis, I contributed to the discovery of novel naevus-associated loci also having a pleiotropic effect on melanoma development. Beyond this, I identified which lipids are dysregulated with age, highlighting a network of lipid-related genes co- and over-expressed in younger individuals, likely under epigenetic regulation. Finally, I discovered that sun-seeking behaviour has a genetic basis, identifying five responsible genomic loci. In this thesis, I have not only helped broaden the knowledge of age-associated melanoma risk factors, I also contributed to the understanding of how an individual's behaviour can be shaped at the genetic level.