We construct a simplified mathematical model of autophagy induction. Autophagy is a catabolic mechanism, present in all living cells, of recycling unnecessary or dysfunctional elements; it also ensures cellular survival during starvation. Autophagy may be induced in response to extra- or intracellular stress and signal. We investigate cell’s response to Rapamycin treatment and starvation via rule based modeling of the known interactions. We find that the modeled system exhibits bistability with two distinguished states: protein synthesis in unstressed cells and autophagy in cells treated with Rapamycin and/or stressed.