In contrast, lung fibroblasts isolated from IPF patient fibrotic foci (IPF fibroblasts) have enhanced PI3K/AKT activity due to PTEN suppression, which causes IPF fibroblasts to have a highly proliferative and apoptosis-resistant phenotype on collagen matrix [24,25]. The gene discussed is AKT1; the disease is idiopathic pulmonary fibrosis.