Therefore, the development of preclinical models for such low‐grade gliomas will inevitably be fraught with the conundrum of low growth rates and therefore make them difficult to fit in a preclinical setting requiring high throughput and short tumour latencies; (d) to develop preclinical models which have a high tumour incidence and a rapid growth, but have to compromise on the genetic makeup of the corresponding human tumour, for example by coexpression of growth factors such as PDGFB or introduction of deletions of tumour suppressor genes such as CDKN2A/B. The gene discussed is CDKN2A; the disease is neoplasm.