In a mouse model of PDAC, depletion of Treg cells results in the functional reprogramming of cancer-associated fibroblast (CAF) populations, resulting in the loss of tumor-restraining α-SMA+ CAFs and tumor outgrowth (Zhang et al., 2020); the loss of Treg cell–derived TGF-β may drive α-SMA+ CAFs to lose their myofibroblastic phenotype, resulting in increased carcinogenesis, the generation of aberrant immune responses, and unrestricted tumor growth. The gene discussed is ACTA1; the disease is neoplasm.