Common, chronic diseases associated with age have common roots. It is now apparent that many such disorders have their origins in the age-related decline of a number of interlinked basic health maintenance mechanisms, termed the ‘hallmarks of ageing’. Our team has discovered a new, and druggable, hallmark of ageing; dysregulation of alternative splicing (AS). Splicing factor expression shows characteristic alterations in normal mammalian ageing, in human primary senescent cells, in cells from individuals with human progeroid syndromes and is predictive of multiple later ageing phenotypes in human populations. Furthermore, targeted restoration of splicing factor expression using small molecules or oligonucleotide therapeutics can attenuate cellular senescence phenotypes. In this presentation, I will outline the background leading to our discovery of dysregulated alternative splicing as a new hallmark of ageing. I will then describe our emerging data demonstrating that it is possible to attenuate splicing factor expression in a partially-senescence specific fashion in human primary cells of multiple lineages using oligonucleotide senotherapeutics, and that by doing so we are able to reverse features of senescence and markers of age-related disease in patient cells from an exemplar ageing disorder IPF and ex vivo in fibrosis-induced living human primary tissues. Drugs that target the regulation of splicing factors may therefore represent promising novel anti-degenerative therapies in the future.