Recent reports revealed that loss of MTAP, a gene flanking and frequently co-deleted with CDKN2A, can render cancer cells sensitive to PRMT5 inhibition, thus opening up opportunities to exploit this vulnerability for treating tumours with MTAP–CDKN2A co-deletion.26 For affected individuals with large deletions involving CDKN2A and MTAP, such as our patient and the family described by Baker et al.,25 the possibility of targeting this PRMT5 dependence raises potential for therapeutic strategies. The gene discussed is CDKN2A; the disease is neoplasm.