Notably, in the pro-fibrotic context, CaSR negative allosteric modulation abrogates this increase in polyamines and the polyamine exporter, SLC3A2, at the transcriptomic level in lung fibroblasts from healthy subjects, and at the molecular level in lung fibroblasts from patients with IPF. The gene discussed is CASR; the disease is idiopathic pulmonary fibrosis.