drug, can be understood in a more simple way as a consequence of a dormant phase. To assess the generic importance of dormancy as an escape strategy we develop a very simple model framework, in which we only focus on the most essential aspects of population and evolution dynamics. 

Here we show that the existence of a dormant phase can be crucial for a population to escape extinction. We consider the following simplified scenario. We study the survival probability of a population of organisms that can exist in the form of three different types, see the diagram 1. The types differ in their response to the presence of a drug. Type (1) and type (2) have similar reproduction and death rates when no drug is present. However, the drug is supposed to be lethal to type (2) but neutral to type (1). We are interested in how the existence of a dormant mode, type (3), effects the survival probability of the entire population. The dormant type cannot reproduce, nor is it susceptible to the drug. However type (3) can die and it can undergo a transformation back to type (1). To understand the effect of the dormant type we consider different realisations (indicated in the diagram 1) of the possible flow between the three different types. 

Our model is relevant to a number of biological cases, in particular to entities such as cancer cells, which have been observed to evolve resistance to therapy: Treatments impose a selective pressure which eliminates the lesser fit strands of the corresponding populations but also drives an evolutionary process whereby better adapted individuals, i.e. individuals immune to the effects of the corresponding drug, eventually take over. Further rationale for our model is provided by the response of tumour cells to hypoxia (i.e. oxygen starvation). It is a well-known fact that hypoxia induces arrest of the cell-cycle [6, 7]. This means that the rate at which cells replicate under hypoxia is drastically reduced, as hypoxia down- regulates the activity of the pathway regulating the progression through the cell-cycle [6]. Moreover, another well-understood fact about cell survival/death regulation is that there exists cross-talk between the pathways regulating cell death and cell division [8–10]. This means that, in normal circumstances, the down-regulation of the cell cycle machinery implies the down-regulation of the apoptotic (programmed cell death) machinery. It can be argued that such cross-talk is disrupted in cancer cells, and that cancer cells are such that cell death regulatory pathways are down-regulated. Therefore, under hypoxic conditions, cancer cells undergo a drastic reduction of their division and death rates. 

The study of the influence of hypoxic cancer cells fits rather well within the original remit 

