The implementation of mechanisms of homeostatic plasticity are thought to provide stability of firing rates in individual cells and thus prevent either silent neurons or runaway excitation, as is the case in epilepsy. These homeostatic mechanisms have been proposed to be implemented in a cell-intrinsic fashion. In this talk, I will describe new data from our lab, which suggest a role for network interactions and inputs to cortical cells in the implementation of homeostatic plasticity, together with classic homeostatic mechanisms. These data also provide further evidence of shifting the balance between excitation and inhibition in the adult visual cortex towards reduced inhibition, as permissive for excitatory functional changes. Thus, both homeostatic mechanisms and network interactions may facilitate the maintenance of activity. Based on these data, I will discuss potential roles for homeostatic plasticity in cortical remodeling, specifically through interactions with Hebbian plasticity, such as long-term potentiation and long-term depression.