These differences in clonal kinetics may reflect the different mechanisms of actions of anti-CTLA4 and anti-PD-1 drugs.11 Infiltration of memory cytotoxic CD4+ and CD8+ T cells has been identified in ICB-induced encephalitis, and recent single cell studies in patients developing colitis irAEs during ICB identify signatures of proliferation and IFNγ responsiveness in colitis-associated T cells.61 62 Our findings of PD-1 and HLA-DR expression on expanded clones of interest are consistent with these reports. The gene discussed is CTLA4; the disease is colitis.