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52) There were no subjects homozygous for the risk T allele in the case of 5HT2A (rs6314) polymorphism and therefore group comparisons were made between TC and CC genotypes. Thus, the overall sample (N=80 [schizophrenia+HCS]) was sub-divided according to the COMT (rs4680), 5HTT (5HTTLPR) and 5HT2A (rs6314) genotypes, irrespective of phenotype viz., COMT: Val/Val+Val/Met vs. Met/Met (i.e., GG+GA vs. AA); 5HTTLPR: S/S+L/S vs. L/L (i.e., SS+LS vs. LL); and 5HT2A: tyrosine-cysteine (TC) vs. cysteine-cysteine (CC). Using a full factorial model in VBM, we examined the interaction between diagnosis and each of the candidate genotypes (COMT [rs4680], 5HTT [5HTTLPR] and 5HT2A [rs6314]). We then carried out exploratory post-hoc comparisons of regional brain volumes between the genotype-wise sub-groups for each of the above 3 polymorphisms. Additive effect of the risk alleles on brain morphometry PERK inhibitor was explored by comparing brain volumes of subjects who had 2 or 3 risk alleles (n=53) of the above 3 risk genes vs. those who had 1 or no risk alleles (n=27). In view of the limited number of subjects having the risk allele T (n=13) we attempted to find the additive effect of the other 2 risk alleles (Val of COMT rs4680 and S allele of 5HTTLPR) after excluding the subjects who were carriers of the T allele of 5HT2A rs6314 polymorphism (n=14) by performing VBM comparison between those subjects having Val allele of COMT and short allele of 5HTT (n=40) I BET151 vs. those subjects having 1 or no risk alleles (n=26) of COMT rs4680 and 5HTTLPR. Age, gender and TBV were entered as nuisance co-variates for all the above analyses. Given the exploratory nature of this study, we used 3 levels of statistical thresholds; initially at a stringent Oxygenase statistical significance threshold of family wise error (FWE) p