Aside from its adaptive potential, germ cell aneuploidy is usually considered a 'mistake' with dire clinical consequences. The prevalence of aneuploidy in spontaneous abortions and various disabling syndromes of liveborn testifies to the importance of abnormal chromosome numbers arising at meiosis. While some fraction of these conditions may be attributable to embryonic chromosomal errors, it is believed that meiotic nondisjunction represents the primary mechanism. Apparently, meiotic trisomies arise from nondisjunction at metaphase I more often than at metaphase II. This is not surprising in view of the unique chromosomal activities occurring in the primary meiocytes which may be vulnerable to alterations predisposing these cells to aneuploidy. At this stage, errors in vibalent formation, crossing over, or segregation may lead to aneuploidy. Secondary meiocyte division is similar to mitosis and presumably is susceptible to the same types of anomalous segregation that can lead to aneuploidy in somatic cells. The intent of the overview is to summarize and integrate some of the current major concepts of meiotic aneuploidy development.