Shaw et al. present striking data showing that the rate of prefrontal cortical thinning is significantly different, indeed almost nonoverlapping, between those with no ADHD symptoms and those who meet full diagnostic criteria, reaffirming the evidence for a neurobiological basis of the diagnosis of ADHD (see Figure). Use of these developmental data as clinical biomarkers for ADHD would be premature, however, until effect size, specificity, and sensitivity as well as the effects of outliers can be fully established. We can also see from Figure 3 in the article that there is considerable overlap in cortical thinning across groups with different levels of ADHD symptoms. This pattern of findings indicates that we have not reached the goal of identifying a marker for ADHD. To put it differently, the developmental differences found in rates of cortical thinning, albeit impressive, do not have clinical implications for the diagnosis or care of individuals with ADHD symptoms. A longitudinal study of children with ADHD (9), who now have been followed at age 41, is relevant to this caveat. The as yet unpublished findings confirm thinner cortices in ADHD subjects than in non-ADHD comparison subjects, including in regions that underpin attentional control. However, there was no difference in cortical thicknesses between those whose ADHD had remitted and those in whom it had persisted, suggesting that the anatomical differences found are not sufficient to explain the clinical phenomenon.