Gravitropism is a process by which plant organs readjust their growth toward or away from the gravity vector when the plant is reoriented. The actin cytoskeleton has often been a significant component of models explaining gravitropism, but its role in this process has become somewhat controversial in light of reports showing that actin inhibitors enhance the gravitropic response. The work with inhibitors implies that actin might function as a negative regulator of gravitropism. In this article, possibilities for how such a role might be accomplished are presented. First, the organization of actin in statocytes is revisited in an attempt to rationalize how compressive forces exerted by statoliths on membranes can lead to enhanced gravity sensing. Second, recent genetic work in the model plant Arabidopsis thaliana is discussed, focusing on the potential involvement of the protein degradation machinery in actin-mediated control of statolith dynamics and on the intriguing possibility that an actin-regulated, ligand-receptor mechanism for gravity signal transduction might operate in higher plants. Third, modifications in the trafficking of auxin efflux transporters are considered as possible mechanisms for the enhanced gravity responses observed in plant organs when the actin cytoskeleton is disrupted by chemical inhibitors. The various possibilities presented in this review emphasize the large amount of research that remains to be done before we can fully understand how the actin cytoskeleton modulates tropisms in higher plants.