In the world of pathogen-host cell interactions, the autophagic pathway has been recently described as a component of the innate immune response against intracellular microorganisms. Indeed, some bacterial survival mechanisms are hampered when this process is activated. Mycobacterium tuberculosis infection of macrophages, for example, is impaired upon autophagy induction and the bacterial phagosomes are redirected to autophagosomes. On the other hand, pathogens like Coxiella burnetii are benefited by this cellular response and subvert the autophagy process resulting in a more efficient replication. We study at the molecular level these two different faces of the autophagy process in pathogen life in order to elucidate the intricate routes modulated by the microorganisms as survival strategies.