Interventions that slow down aging provide invaluable insights into its causes. But do they act upon common underlying mechanisms? Recent work with a long-lived mutant mouse, the Ames dwarf, showed that its life-span could be further extended by another intervention, dietary restriction, in which food intake was restricted to about 70% of voluntary levels. This finding was taken to demonstrate that the Ames mutation and dietary restriction slow aging by different mechanisms, because the Ames mutation and dietary restriction do not mask each other's effect on life-span. Using the fruit fly Drosophila, we show here that (i) slowing of aging by a mutation in an insulin/insulin-like growth factor (IGF)-like signaling (IIS) pathway and by dietary restriction occurs by overlapping mechanisms and (ii) life-span must be maximized by at least one of the interventions under investigation for a proper test of the hypothesis that the mechanisms of life-span extension differ.