Schizophrenia is a highly complex and disabling disorder with heritability estimates as high as 80% (Sullivan et al., 2003). The genetic risk of schizophrenia established from twin/family studies, and genome wide association studies denote a complex polygenic architecture with several common (108 candidate regions) and rare variants contributing to schizophrenia susceptibility (Rees et al., 2015). Clinically, schizophrenia is heterogeneous with wide variations in symptom presentation. Despite advances in technology that facilitate biological inquiry, pathogenic mechanisms of schizophrenia still remain largely unknown. Heterogeneity at the clinical level and complexity at the molecular level have been cited as strong reasons for this (Rasetti and Weinberger, 2011). In an attempt to address these challenges, some studies have focused on a sub-phenotype approach to examine molecular mechanisms of symptoms (Fanous et al., 2012). This is a validated approach and there is growing evidence for its utility in advancing the field (Jones et al., 2016; Sengupta et al., 2017).
