Though initially conceptualized as resulting from peer imitation of child-onset or life-course-persistent youth [Moffitt, 1993], there is mounting evidence from twin studies that adolescent-onset or adolescent-limited antisocial behavior may also be genetically influenced. This study sought to provide preliminary molecular genetic evidence in support of these findings. We further evaluated whether genetic associations varied between behavioral subtypes of ASB (i.e., physical aggression and nonaggressive rule-breaking), given that only the latter has been found to characterize adolescent-onset ASB. The sample consisted of 211 undergraduate men of European-American ancestry. Three polymorphisms with theoretical and/or empirical ties to ASB or related traits (i.e., tryptophan hydroxylase-A218C, 5HT(2A) His452Tyr, and the DAT1 variable nucleotide tandem repeat) were genotyped. Analyses revealed that two of the three polymorphisms (i.e., His452Tyr and DAT1) were associated with adolescent ASB. Moreover, these associations appeared to be specific to the nonaggressive, rule-breaking form of ASB, and did not extend to physical aggression, further supporting ties to adolescent ASB in particular. Such results thus constructively replicate earlier findings of genetic influence on adolescent ASB. They also offer preliminary evidence that the genetic processes underlying aggressive and nonaggressive antisocial behavior may be (at least partially) distinct.