Ras activates Raf. It can not be turned off. So this is a classic oncogene. The other main way to achieve cancerous transformation is by mutation in Tumor suppressor genes - about 10 have been identified. Their normal function is to constrain cell growth.
Mutations release the cell from the constraint.
Turned out the DNA they used was mutant p53. It works to prevent tumor formation. When it is mutated, a tumor forms. If DNA damage can activate an oncogene, then p53 will try to solve the problem, either by preventing mitosis until repair can be attempted, or if it's too late, to kill the cell before a tumor can form. At a certain point in the maturation of a cell, telomerase shuts off and our telomeres get shorter and shorter with every round of cell division.