Different classes of carcinogenic agents may independently produce somatic mutations leading to malignant growth. There are reasons for believing that chromosomal rather than point mutations are involved, and for concluding that these might result from nuclease activation rather than direct interactions of carcinogens with genetic material. The lysosomes, as the main repositories of endonucleases in most mammalian cells, may therefore assume significance in carcinogenesis. Evidence is adduced that chemical and physical agents and viruses all have effects on lysosomes. Selective damage to lysosomes seems to be associated with an increased malignant potential in cultured cells. Children with congenitally abnormal lysosomes (Chédiak-Higashi syndrome) tend to develop reticuloses. Children with Bloom's syndrome or Fanconi's anaemia also have greatly increased susceptibility to malignancy, and their cells frequently show chromosome breakage and other aberrations in culture. Lysosomal changes have also been reported in the cells of tumours treated with Cytoxan or X-irradiation.