In their commentary, Manuel Cuesta and Víctor Peralta [1] acknowledge several of the basic contributions and challenges of our SyNoPsis project. They appreciate the attempt to link clinical manifestations with the neurobiology of schizophrenia by means of a revised semiology, and the proposal to understand its essence as a disorder of interpersonal communication. The authors also recognize the aspects contributed by the important work of Carl Wernicke and Karl Leonhard [2,3]. Also, they carve out some relevant limitations of SyNoPsis. Although a relationship of specific symptom dimensions to the respective sensorimotor and corticostriatal brain systems has been shown in several studies [4], the functional specificity of these systems has yet to be defined [5]. Further, different within-systems dynamics may result in different symptom patterns, and the anatomical connections and functional interactions between the systems have not yet been sufficiently understood.In their commentary, Cuesta and Peralta raise two critical clinical aspects: the course of the illness, and the representation of negative symptoms. We agree that the course of psychotic disorders is of eminent importance for clinical management, but also for understanding the long-term dynamics of the brain systems involved. In fact, our clinical instrument, the Bern Psychopathology Scale (BPS) [6], was designed as an instrument for crosssectional assessment. However, it allows recurrent assessments at deliberate intervals for follow-up observations. First retrospective studies have recently been published [7], and the issue of the course of psychosis dimensions will be addressed in detail in future projects.Regarding negative symptoms, we pursued a novel approach, mapping "negative" behavior onto inhibitory states of the respective brain functions. Following our objective to revise the semiology of psychosis based on the best of our knowledge about the related brain functions, this group of symptoms was disentangled respecting the boundaries of higher brain functions. For instance, we conceptualize alogia as "inhibition of verbal expression," and avolition as "lack of spontaneous actions." Thus, negative symptoms are redefined according to the tripartite symptom structure of SyNoPsis to match dysfunctions of the three brain circuits in question. In fact, most overlap was found between the motor dimension and negative symptoms [8].