The effects of organ teratogens during fetal development are known to be highly dependent on their timing. In the well-known example in humans, the hypnotic, thalidomide, is only effective as a teratogen during one week of the first trimester of gestation. The resultant teratogenic effects are specific and recognizable. The details of the timing and mechanism of teratogenic events have been most elegantly elucidated in the fruit fly, Drosophila Melanogaster (Schlesinger, Ashburner, & Tissieres, 1982). In this model the most commonly studied teratogen has been heat shock. During a period of rapid gene expression of some bodily part of the larvae (such as the wings or legs), the development of that particular bodily part is highly sensitive to the effects of heat shock. In these critical periods, or developmental windows, the gene expression of the particular part of Drosophila is put on hold by heat shock or other teratogens. When the environmental danger to the cells is past, the genes begin to express normally again, but they do not return to the previous cycle of gene expression to correct omissions or developmental errors. Each part of the body of Drosophila has a narrow developmental window of its own. Thus, if the heat shock is presented during the 37 to 41 hours of the pupal stage, the resultant Drosophila may have no wings, or the wings may be deformed. If the heat shock is presented during the 40 to 44 hours of pupal development, the head will not develop properly. The part of the larva that develops abnormally depends on which part happens to be experiencing a spurt of gene expression and development at the time of the teratogenic event.