This is in contrast with the prediction for independent mechanisms, where observations of modifications are less informative about reprogramming times. It’s known that different types of 
cells have different reprogramming potential. In our work we examine the influence of the existence of subpopulations of cells in reprogramming dynamics. We studied the scenario where cells are all equal at induction but accrue differences due to stochastic events, and the scenario where there are subpopulations of similar cells with different epigenetic features. In both cases we illustrate how cellular state, acquired or pre-existing, can lead to elite-type behavior and cause significantly different reprogramming times. This, in our predictions, is especially true for the cooperative mechanisms and particularly when dominated by slow steps. Slow steps can create kinetic barriers to reprogramming that may create the appearance of elite behavior. Kinetics and mechanisms also have an important impact when the desire is to accelerate reprogramming protocols. If the process is dominated by a Pimozide single slow reaction, then accelerating that reaction is the key to improving efficiency. If the process is dominated by several slow steps, then accelerating only one of them has a smaller effect and one might consider having to accelerate several of them �C in which case the order of intervention for acceleration becomes important. Recent studies suggest that SOX2 has a specific time window of action. In light of our results, this is consistent with the hypothesis of a mechanistically ordered system of modifications on the path to reprogramming. Further, it raises the possibility that the action of this transcription factor is one of the limiting steps for reprogramming. Naturally, only with further experimentation can this be confirmed. Possible experiments include inhibiting specific steps to determine whether those steps are part of an ordered mechanistic chain of events or an unordered process. If a step is part of an ordered necessary path, then inhibiting it will trap cells in that state; on the other hand, if a step is part of an unordered Benzethonium Chloride mechanism then inhibiting it will not impede progress along other necessary modifications. Similar to the work done with SOX2 there are also recent indications that the timing of action for promoting DNA demethylation is an important feature, and recent work showing that cells can become trapped due to-non completion of this step. Once again, our work suggests that one explanation for these observations might be that this epigenetic modification is part of an ordered cooperative mechanism of changes with more than one slow step. Given these observations and recent developments that indicate the possibility of substituting factors for reprogramming with small molecules, as well as recent work describing screening approaches that were used to inhibit the action of specific kinases important for the reprogramming process, we suggest that experiments with time-dependent screening of inhibition or acceleration of particular steps might be used to understand not just what steps are limiting, but also the mechanistic dependencies between the several key steps of the reprogramming process. Besides suggesting a different take on the elite versus stochastic framework proposed by Yamanaka, we believe that work presented here will help increase the efficiency of cellular programming. Indeed, as illustrated, certain types of data about the times of milestone events and subsequent analysis can reveal kinetic and mechanistic information about the process of cellular reprogramming.