Since increases in [Ca2+]i underpin key fibrotic processes, such as activating genes responsible for the production of TGFβ, collagen, and α-smooth muscle actin (αSMA) in fibroblasts [56], our findings suggest a potential pathophysiological interplay between polyamines, the CaSR and Ca2+i, which may contribute to IPF development. The gene discussed is ACTA1; the disease is idiopathic pulmonary fibrosis.