It was felt that Src was a good candidate for knock-down because: 1) elevation of Src activity has been implicated in the development and/or progression of human cancer, 2) efficient knock-down of Src is unlikely to cause impairment of normal cells, as Src knockout mice are viable [16]; and 3) it is unlikely that complete knock-down of Src would be required to elicit a cellular effect on cancer cells, as low levels of Src activity are present in most normal cell types. This evidence concerns the gene SRC and cancer.