Family and twin studies have consistently reported high heritability for schizophrenia. Heritability was high and the relative risk (RR) was consistent with prior reports indicating a strong genetic component to schizophrenia. Progress has been made with large-scale genome-wide association studies (GWAS) contributing important initial evidence of replicable schizophrenia risk alleles, in the form of single nucleotide polymorphisms (SNPs). Cognitive impairment has long been recognized as a core feature of schizophrenia, with significant, diffuse dysfunction that includes intellectual deterioration as well as more specific deficits in individual cognitive domains, such as working memory and executive functioning. Neurocognitive dysfunction has received substantial attention as a candidate endophenotype in schizophrenia and may be particularly useful in the context of large-scale molecular genetic studies. Inheritance of attentional deficits in schizophrenia has typically been measured by various continuous performance tasks.