Attempting to explain aging by a single factor was the weakness of most theories. G.A. Sacher proposed a synthetic theory named the longevity-assurance theory. Here, I propose a revised version of it. A comprehensive phylogenic tree based on molecular biology is available for organisms including bacteria, plants, protozoa, fungi, insects and vertebrates. Combining this tree with classical data, we conclude that land plants evolved from immortal, gigantic plants to perenials and then annuals, i. e., from the giant to the miniature. In animals, too, the number of present-day species exponentially increases with decreasing body length except for very small insects. Organisms of smaller size usually have shorter lifespans and earlier maturations, resulting in more success in the reproduction. Annual plants and insects are genetically programmed to die shortly after production of offspring. Genes for programmed death or division arrest are senescence genes. They were acquired by annual plants and insects to assure successful production of offspring. However, mammals evolved toward the opposite direction from small ancestral animals to larger ones of various sizes. There is an empirical rule that mammalian species of greater body-weight have longer lifespans and lower values of specific metabolic-rate (cal/g/day). These results support the explanation that metabolisms themselves produce senescence-accelerating toxins, presumably free radicals. Most primates have two-fold longer lifespans than most other mammals when compared at comparable specific metabolic-rates. This indicates that primates have specifically advanced longevity-assurance mechanisms. In fact, cultured human fibroblasts are unbelievably resistant to malignant transformation whereas cultured rodent fibroblasts are easily transformed. When cultured in vitro, human fibroblasts always stop the DNA synthesis after a limited number of cell division; they nerver produce immortal clones. Around the time of entering senescence, fibroblasts begin to produce DNA-synthesis-inhibiting proteins. Most human tumor cell-lines are defective at genes that produce inhibiting proteins. Thus, senescence genes work for anti-tumor mechanisms. Even if a single aged cell becomes immortal within the body, it will be a potential cause of tumorigenesis or autoimmune disease. Absolute altruism is the rule for the behavior of individual cells in the animal body. Evidence is avilable that various types of cells frequently die by activating senescence genes for the maintenence of the whole-body's function. Thus, senescence genes are involved in altruistic suicide of cells to assure longevity of the host. In Drosophila melangogaster, senescence genes to inhibit post-larval DNA synthesis are mapped at more than 20 loci. One of them has recently been cloned and identified as a gene coding for a cell-membrane adhesion protein. Cloning of senescence genes is opening up an exciting new field in gerontology.