Cancer develops when cells no longer follow their normal pattern of controlled 
growth. In the absence or disregard of such regulation, resulting from changes 
in their genetic makeup, these errant cells acquire a growth advantage, 
expanding into precancerous clones. Over the last decade, many studies have 
revealed the relevance of genomic mutation in this process, be it by 
misreplication, environmental damage, or a deficiency in repairing endogenous 
and exogenous damage. Here, we discuss homologous recombination as another 
mechanism that can result in a loss of heterozygosity or genetic rearrangements. 
Some of these genetic alterations may play a primary role in carcinogenesis, but 
they are more likely to be involved in secondary and subsequent steps of 
carcinogenesis by which recessive oncogenic mutations are revealed. Patients, 
whose cells display an increased frequency of recombination, also have an 
elevated frequency of cancer, further supporting the link between recombination 
and carcinogenesis.