This paper reviews our present state of knowledge of genetic variation in (offensive) aggression in wild house mice. The basic tools in this research were lines bidirectionally selected for attack latency (fast attacking SAL and slow attacking LAL males), descended from a feral population. Using congenic lines for the nonpseudoautosomal region of the Y chromosome (YNPAR), reciprocal crosses between (parental) SAL and LAL, and crosses between parentals and congenics, an autosomally dependent Y chromosomal effect on aggression has been found. Both the pseudoautosomal (YPAK) region and the YNPAR play a role. As for environmental sources of variation, prenatal and postnatal maternal effects are of minor importance for the development of aggression differences. One of the physiological factors by which genetic effects may be mediated is testosterone (T). Besides quantitative aspects, the timing of T release seems crucial. Two important time frames are discussed: the perinatal and pubertal time periods. Finally, neurochemical and neuroanatomical correlates are considered. Differences in neostriatal dopaminergic activity, and sizes of the intra- and infrapyramidal mossy fiber terminal fields, as well as Y chromosomal effects on the latter two, are discussed.