“…As a result of the work of many laboratories on sev eral different model systems, there is no lon ger any doubt that longevity and senescence are under some form of genetic control [2], In the case of Drosophila, this statement is based on evidence obtained from a variety of studies using single gene mutants, transgenic animals, and/or selected strains. Several laboratories have used various reproductive selection schemes to derive genetically selected longlived and/or short-lived strains from a progen itor baseline, and have interpreted their re sults as a conclusive demonstration that lon gevity is a malleable phenotype amenable to genetic analysis [3][4][5][6][7], In a recent communication, Baret and Lints [8] have reinterpreted certain selected strain data in an effort to demonstrate a dis senting view: namely, that '... the mean longe vities of a series of lines, presumably geneti cally different -if we admit that indirect selection by late reproduction has some effect on the gene pool -do not differ after 21 gener ations of selection' [8, p. 257], that '... the dif ferences between lines may be explained simply by the time lag in the measurements of the longevity' [8, p. 259], and thus that 'kind of experiment appears now to be irrelevant to Introduction test the genetic determinism of longevity in D. melanogaster' [8, p. 259], They arrived at this conclusion by taking a limited set of data from the experiments of Lints and Hoste [9], Luckinbill et al [4] and from Luckinbill and Clare [10], and then replotted the calculated mean longevities as a function of the number of days elapsed since the beginning of the selection experiment, rather than by the more conventional method of plotting the longevi ties as a function of the number of generations elapsed since the initiation of selection. Their rationale for adopting this new procedure is to compensate for the time lag that inevitably appears between the measurements of a given generation in early or late lines.…”