demonstrated that TGFβ2 is highly expressed in the lungs of idiopathic pulmonary fibrosis (IPF) patients owing to its lower activation threshold than that of TGFβ1, elucidating a distinct role of TGFβ2 in the progression of IPF.[37] This aligns with our hypothesis that, under estrogen‐deficient conditions, TGFβ2 upregulation precedes that of TGFβ1 to mediate initial responses as the starting point for the fibrotic cascade in the SG. The gene discussed is TGFB1; the disease is pulmonary fibrosis.