While Tregs are known suppressors of anti‐tumor immunity in PDAC, they comprise a heterogeneous population with distinct functional subtypes.[23] For instance, in ovarian cancer, effector Tregs (eTregs) were shown to mediate the therapeutic response to PARP inhibition,[24] while in lung cancer, OXhiGITRhi Treg were associated with resistance to PD‐1 blockade.[25] Based on these insights, we focused on Treg subclusters rather than total Treg abundance. The gene discussed is PDCD1; the disease is lung carcinoma.