"Oncogene addiction" describes the curious acquired dependence of tumor cells on 
an activated oncogene for their survival and/or proliferation, a phenomenon that 
has important implications for the success of targeted cancer therapies. 
However, the mechanisms explaining oncogene addiction remain elusive. We propose 
that "addiction" may be an illusion generated as a consequence of differential 
attenuation rates of prosurvival and proapoptotic signals emanating from an 
oncoprotein acutely following its inactivation. According to this model, which 
we call "oncogenic shock," prosurvival signals dissipate quickly on oncoprotein 
inactivation whereas proapoptotic signals linger sufficiently long to commit the 
cell to an apoptotic death. This mechanism may contribute to the rapid and 
dramatic clinical responses observed in some cancer patients treated with 
selective tyrosine kinase inhibitors and could yield additional drug targets 
that determine the balance of signaling outputs from activated oncoproteins.