The ACE estimates for P300 amplitude reported above (A:0.63; E:0.36) represent the genetic and environmental contributions to P300 amplitude on average across all levels of AAU in our sample. Figure 4a visually presents the ACE estimates for P300 amplitude as calculated from the Endophenotype model. The Alcohol Exposure model, on the other hand, produces estimates of the G-E influences on P300 amplitude as a function of AAU. To the extent that such changes are present, the Alcohol Exposure model would provide a significantly better fit to the data than the Endophenotype model. As indicated in top portion of table 2, the -2LL, AIC, BIC, and DIC comparisons all fail to support the Alcohol Exposure model as providing the better fit to the observed data, suggesting that the genetic and environmental influences on P300 amplitude do not vary with AAU. Figure 4b visually presents the ACE estimates across the range of AAU scores as calculated in the Alcohol Exposure model. As shown, the sum of the ACE estimates slightly decreased from low to high levels of AAU, due mostly to a