Astrogliosis, characterized by the enhanced expression of GFAP, represents a remarkably homotypic response of astrocytes to all types of injuries of the CNS, including injuries of the developing CNS. As such, astrocytes serve as microsensors of the injured microenvironment regardless of their location in the CNS. The diversity of insults that engender astrogliosis and the brain-wide nature of the astrocytic response suggest that common injury factors serve as the trigger of this cellular reaction. One prominent theme that has emerged in recent years is that proinflammatory cytokines and chemokines serve as a stimulus for induction of astrogliosis. Here we present a brief critique of this hypothesis based on a review of literature and some of our own recentfindings. Studies of astrocytes, in vitro, clearly indicate that these cell types are responsive to a variety of growth factors, including cytokines and chemokines. A somewhat different picture, however, can be seen from data obtained in vivo. It is true that trauma and diseases of the nervous system, as well as some exposures to neurotoxic chemicals, can be associated with the expression in brain of large varieties of cytokines and chemokines. That these same conditions result in astrogliosis has fostered the circumstantial link between cytokine/chemokine expression and the induction of astrogliosis. Several lines of evidence argue against this view, including (a) suppression of cytokine expression does not suppress gliosis, (b) gliosis can occur in the absence of enhanced expression of cytokines, (c) elevations in brain cytokines can occur in the absence of gliosis and (d) the patterns of cytokine expression in the adult and developing CNS are more consistent with a trophic role for these chemical messengers rather than a role in the induction of inflammation. Enhanced expression of cytokines and chemokines after brain injury appear to be signal transduction events unrelated to the induction of astrogliosis.