fair, (2 (20) = 313.94, AIC = 345.9, CFI = .786, SRMR = .149), suggesting that there were nuances in the genetic architecture not fully captured by a single cross-trait index of genetic risk. An exploratory factor analysis (EFA) of the S matrix with three-factors using the promax rotation in the R package factanal was then used to guide construction of a follow-up model (Table S2.2). A follow-up confirmatory model with three correlated factors was specified in Genomic SEM based on the EFA parameter estimates (positive standardized loadings > .2 were retained; Figure 2b). This model provided good fit to the data (2 (15) = 85.35, AIC = 127.36, CFI = .945, SRMR = .079). Results indicated there was a moderate genetic correlation between the compulsive and mood/psychotic disorders factors (rg = .43, SE = .08), a smaller genetic correlation between the mood/psychotic and early onset factors (rg = .25, SE = .05), and next to no correlation between the compulsive and early onset factors (rg = < .01, SE = .07). A model that included additional negative cross-loadings provided similar fit to the data and highly similar correlations across the genetic factors. Given this consistency in results, the correlated
