For example, preclinical models are expected to discover the molecular and cellular mechanisms of cognitive deficits in schizophrenia, such as cerebral organoids derived from human embryonic stem cells and patient-derived induced pluripotent stem cells from schizophrenia, which are able to clarify the pathogenesis of cognitive deficits and the role of brain insulin resistance to exclude the effects of antipsychotics on this relationship. This evidence concerns the gene INS and schizophrenia.