The genesis of actinic keratoses (AK) is complex, involving both environmental and genetic factors. One of the main environmental factors is excessive exposure to UV light. There are several pathogenetic mechanisms that actinic keratoses progress through; the most significant ones include inflammation, oxidative stress, immunosuppression, altered apoptosis, dysregulation of the cell cycle, cell proliferation, and tissue remodeling. The molecular basis of disease progression from UV-induced precancerous actinic keratosis to malignant invasive cutaneous squamous cell carcinoma (cSCC) and potentially fatal metastatic disease has been linked to a number of transcriptional factors, tumor suppressor proteins, and growth factors. Dermoscopy is usually used in a clinical diagnosis of actinic keratoses, providing a high degree of specificity and sensitivity. Although it is impossible to predict with certainty which AKs will progress to SCC, major clinical risk factors may include rapid enlargement (>1 cm), bleeding, erythema, ulceration, induration, and inflammation. Preventing the disease is the first step in halting its occurrence.