On one hand, early activation of TGF‐β and EMT can promote inflammation resolution and tissue regeneration by enhancing cell migration, inhibiting cell death and senescence, and supporting cell dedifferentiation.[54, 55] On the other hand, sustained or excessive TGF‐β and EMT activity has been implicated in fibroblast activation, extracellular matrix deposition, and ultimately pulmonary fibrosis.[81, 82, 83, 84] In our study, the early activation of these pathways after FLASH irradiation coincided with reduced inflammation, suggesting an acute shift toward tissue repair and homeostasis. The gene discussed is TGFB1; the disease is pulmonary fibrosis.