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Pharmacological MRI studies rely on the assumption that haemodynamic measures can be considered a proxy of altered neurotransmission. However, the fMRI signal has no intrinsic selectivity to any particular receptor sites and the degree to which haemodynamic response indexes the action at drug target sites is still an open question. To address this issue, we developed REACT (Receptor-Enriched Analysis of functional Connectivity by Targets), a multimodal method that enriches the resting state fMRI analysis with the molecular information about the distribution density of specific receptors in the brain. With this new approach, we are able to show that drug-induced functional effects can be understood through the distribution of their main targets.