Telomere shortening in humans can induce replicative senescence, which blocks cell division. Cancer cells avoid replicative senescence to become immortal. In this G state, neurons continue functioning until senescence or apoptosis. BRAF and Ras are two oncogenes implicated in cellular senescence. These results highlight the independence of cellular senescence from epigenetic aging. Greider also worked with Calvin Harley to show that telomere shortening underlies cellular senescence (1990). The therapy can also eliminate cancer cells by inducing androgen deprivation-induced senescence. This process is known as "replicative senescence", or the Hayflick limit. This protein may play a role in cell growth, senescence, and differentiation. Colibactin can cause cellular senescence or cancer by damaging DNA. Progeroid syndromes are all examples of aging diseases where cell senescence appears to be implicated. JA can interact with many kinases and transcription factors associated with senescence. Biomarkers of cellular senescence have been shown to accumulate in tissues of older individuals. Essentially, aging-associated diseases are complications arising from senescence. Progeria is another example of a disease that may be related to cell senescence.