The extended survival we observed may be attributable to several factors including (i) the metabolic interactions with the tumour microenvironment, demonstrated in a model of ovarian cancer, where inhibition of stromal glutamine synthetase as well as tumour glutaminase were required to reduce tumour burden [89], (ii) curtailment of metastasis, as demonstrated in neuroblastoma xenografts following PRMT5 inhibition [14] and (iii) immune responses arising from neoantigens following mRNA splicing [90]. The gene discussed is PRMT5; the disease is neoplasm.