In the past 10 years, our laboratory has proved the shine-through paradigm to be a very sensitive endophenotype for schizophrenia. The shine-through paradigm is a visual backward masking task, where the target is a vertical vernier followed by a 25-element grating mask that decreases target discriminability. Behaviorally, we have shown that: 1. Schizophrenia patients and schizoaffective patients show strong and reproducible masking impairments, which are state-independent (Chkonia et al., 2010, 2010b; Herzog et al., 2004). 2. Patients using atypical medication performed better than those treated with typical neuroleptics (Fernandes et al., 2019); 3. Masking impairments are already present in adolescents with psychosys and with first-episode psychosis (Holzer et al., 2004, 2009; Favrod et al., 2018); 4. Performance of unaffected relatives of schizophrenia patients is in between that of patients and controls (Chkonia et al., 2010b; da Cruz et al., 2020); 5. Healthy students scoring high in schizotypal traits also show masking deficits (Cappe et al., 2012; Favrod et al., 2017). Neurophysiologically, masking deficits of schizophrenia patients, patients with first-episode psychosis and students scoring high in schizotypal traits are reflected in decreased global field power amplitudes of the N1 component at 200ms after target onset (Plomp et al., 2013; Favrod et al., 2017; Favrod et al., 2018). We found evidence for a neural compensation mechanism in unaffected siblings of patients as revealed by higher N1 amplitudes than controls (da Cruz et al., 2020). Genetically, one SNP of the cholinergic system correlated well with masking deficits in schizophrenia patients (Bakanidze et al., 2013). Since the boundaries to other psychiatric disorders are poorly defined (Craddock and Owen, 2010), we started to test the shine-through paradigm in patients with psychiatric disorders other than schizophrenia. This allows to determine whether the endophenotype is specific to schizophrenia or to its spectrum. We have shown that: 1. Bipolar patients, similarly to schizophrenia patients, show masking deficits and strongly reduced N1 amplitudes compared to controls (Chkonia et al., 2012; Garobbio et al., 2021); 2. Depressive patients do not show masking deficits although they show reduced N1 amplitudes compared to controls but stronger than schizophrenia patients (Favrod et al., 2019). We propose that impairments in the shine-through paradigm across the schizophrenia spectrum are not caused by visual deficits per se but are related to an interaction between target enhancement (Herzog et al., 2013) and how much intrinsic effort is put in the task (Favrod et al., 2019). On one hand, masking deficits might occur because schizophrenia patients and patients with bipolar disorder cannot enhance the neural responses to the target vernier due to a general dysfunction in attention, recurrent processing and/or neuromodulation (e.g., the cholinergic system). On the other hand, depressive patients can stabilize the neural representation of the target making it less prone to masking, and their low amplitudes might represent less intrinsic effort. Finally, siblings of schizophrenia patients may engage more effort allowing them to recruit more neural resources to partially compensate for their behavioral deficits. These findings close the loop between genetics, neural processing and behavior.