Despite complex genomic and epigenetic abnormalities, many cancers are 
irrevocably dependent on an initiating oncogenic lesion whose restoration to a 
normal physiological activation can elicit a dramatic and sudden reversal of 
their neoplastic properties. This phenomenon of the reversal of tumorigenesis 
has been described as oncogene addiction. Oncogene addiction had been thought to 
occur largely through tumour cell-autonomous mechanisms such as proliferative 
arrest, apoptosis, differentiation and cellular senescence. However, the immune 
system plays an integral role in almost every aspect of tumorigenesis, including 
tumour initiation, prevention and progression as well as the response to 
therapeutics. Here we highlight more recent evidence suggesting that oncogene 
addiction may be integrally dependent upon host immune-mediated mechanisms, 
including specific immune effectors and cytokines that regulate tumour cell 
senescence and tumour-associated angiogenesis. Hence, the host immune system is 
essential to oncogene addiction.