The recent review article on Toxoplasma gondii and neu-ropsychiatric diseases is very interesting [1]. Fabiani et al. [1] reviewed the relationship between T. gondii and neu-ropsychiatric diseases, and mentioned some possible mechanisms of T. gondii that might contribute to the eti-ology of neuropsychiatric diseases. Moreover, Fabiani and his colleagues briefly remarked ''strain's parasite, timing and source of infection, and genetic host factors represent potential links between infection with T. gondii and neu-ropsychiatric diseases''. However, i would like to comment on the importance of parasite strains in the intensity of alterations induced by T. gondii and its roles in the etiology of neuropsychiatric diseases. T. gondii consists of three main genotypes with some differences in virulence and epidemiological patterns. Strain I has higher virulence than strains II and III. Strains I and II have been observed in AIDS patients and congenital infections, whereas strain III is more prevalent in animals [2]. In vitro and in vivo studies also showed variations in these strains [3–5], for example, gene expression in cells infected with strain I was higher than strains II and III [4, 5]. Remarkably, an in vitro study in neuroepithelial cells showed that not only gene expression in cells infected with type I was higher than the two other but also infection with type I mostly affects those genes related to the central nervous system functions [3]. More-over, there are evidences that the type I of T. gondii is more involved in the course of psychotic disorders. In this regard, Xiao et al. [5] observed that the risk of developing adult schizophrenia and psychotic disorders in children's of pregnant women infected with strain I T. gondii was sig-nificantly higher than unaffected controlled mothers (OR = 1.94; p = 0.03). Groër et al. [6] also found that the risk of anxiety and depression was increased in pregnant women with higher titers of T. gondii IgG antibody. Inter-estingly, the depression and anxiety scores were highest in women with serotype I. Furthermore, the difference between two subtypes of strain II in induction of behavioral alterations was observed in a mouse model [7]. In conclusion, among many factors connecting T. gondii and neuropsychiatric diseases, parasite strains play a piv-otal role in the intensity of alterations induced by T. gondii. Hence, strain hypothesis offers a new insight about the role of T. gondii in the etiology of neuropsychiatric diseases. Conflict of interest I declare that I have no conflicts of interest.