An important assumption of our current understanding of the mechanisms of 
carcinogenesis has been the belief that clarification of the cancer process 
would inevitably reveal some of the crucial mechanisms of normal human gene 
regulation. Since the momentous work of Bishop and Varmus, both the molecular 
and the biochemical processes underlying the events in the development of cancer 
have become increasingly clear. The identification of cellular signaling 
pathways and the role of protein kinases in the events leading to gene 
activation have been critical to our understanding not only of normal cellular 
gene control mechanisms, but also have clarified some of the important molecular 
and biochemical events occurring within a cancer cell. We now know that 
oncogenes are dysfunctional proto-oncogenes and that dysfunctional tumor 
suppressor genes contribute to the cancer process. Furthermore, Weinstein and 
others have hypothesized the phenomenon of oncogene addiction as a distinct 
characteristic of the malignant cell. It can be assumed that cancer cells, 
indeed, become dependent on such vital oncogenes. The products of these vital 
oncogenes, such as c-myc, may well be the Achilles heel by which targeted 
molecular therapy may lead to truly personalized cancer therapy. The remaining 
problem is the need to introduce relevant molecular diagnostic tests such as 
genome microarray analysis and proteomic methods, especially protein kinase 
identification arrays, for each individual patient. Genome wide association 
studies on cancers with gene analysis of single nucleotide and other mutations 
in functional proto-oncogenes will, hopefully, identify dysfunctional 
proto-oncogenes and allow the development of more specific targeted drugs 
directed against the protein products of these vital oncogenes. In 1984 Willis 
proposed a molecular and biochemical model for eukaryotic gene regulation 
suggesting how proto-oncogenes might function within the normal cell. That model 
predicted the existence of vital oncogenes and can now be used to hypothesize 
the biochemical and molecular mechanisms that drive the processes leading to 
disruption of the gene regulatory machinery, resulting in the transformation of 
normal cells into cancer.