Our studies show that: (1) polyamine levels are increased in the saliva of IPF patients; (2) polyamines directly act at the CaSR, a receptor expressed in normal and IPF human lung fibroblasts, leading to a rise in intracellular calcium concentration; (3) TGFβ1 upregulates the expression of both polyamines and CaSR in NHLFs, and polyamines only in IPF fibroblasts; and (4) CaSR inhibition with NAM abrogates the key effects of pro-fibrotic stimuli in both normal and IPF HLFs, suggesting that the CaSR and NAM might hold therapeutic potential for the treatment of IPF. This evidence concerns the gene TGFB1 and idiopathic pulmonary fibrosis.