Integration of genomic profiling and clinicopathologic features identifies 3 distinct types of PTLD-CNS. (A) Oncoprint of genomic profiling results and clinical data from the PTLD-CNS cohort. Stratification was performed according to EBV status by in situ hybridization, presence or absence of systemic extra-CNS involvement, and pathogenic molecular alterations involving RAS family oncogenes (HRAS and NRAS) and known lymphoma oncogenes and tumor suppressor genes (MYD88, CD79B, KMT2D, and CDKN2A). (B) Kaplan-Meier survival analysis of patients with PTLD-CNS stratified by Ki-67 LI using a cutoff of 80%.