Abstract
p16(INK4a) (CDKN2A) is a central tumor-suppressor and activator of senescence. We recently found that prolonged expression of p16(INK4a) in epidermal cells induces hyperplasia and dysplasia through Wnt-mediated stimulation of neighboring keratinocytes. The study suggests a pro-tumorigenic function of p16(INK4a) in early epidermal lesions, which could potentially be targeted by senolytic therapy.