CDKN2A and neoplasm: [16], [17] CDKN2A expression is elevated as a function of increasing cellular stress and organismal ageing. As such, this typically accompanies the telomere shortening observed during normal human ageing. CDKN2A acts as a tumour suppressor, is a component of STASIS (stress and stimulation induced senescence) [18] and is functionally involved in maintaining cells in a state of growth arrest. It has previously been demonstrated to be a significant pre-transplant predictor of post transplant renal allograft function [6], [7], [19].