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Exposure to ultraviolet radiation induces two of the most common DNA mutations known in cellular biology. Those include cyclobutane–pyrimidine dimers (CPDs) and 6–4 photoproducts (6–4PPs) and their Dewar valence isomers.[6]. Cells have developed a number of repair mechanisms to counteract the DNA damage caused by ultraviolet radation and other toxins. In human cells, a repair process is initiated after DNA damage is detected in which the damaged DNA is removed before it is replicated. As humans age, their cellular repair mechanisms make more errors because they have accumulated years of oxidative stress from daily life.[7]. Over time, it is more difficult for the cell to find and destroy aberrant DNA. The replication of damaged DNA leads to cancer, and exposure to UV radiation sets a process in motion that can take decades to ultimately cause skin cancer[8]. Similarly, most people who smoke cigarettes do not get lung cancer until decades of use have passed. Most critically, if a mutation occurs within a gene that regulates cell division, the cell becomes prone to malignancy. For example, squamous cell carcinoma (a type of skin cancer) is caused.