Experimental studies analysing IPF and systemic sclerosis fibroblasts showed that persistence of myofibroblasts and resistance of apoptosis are TGF-Β1 mediated mechanisms via the activation of the focal adhesion kinase (FAK)-protein kinase B (PKB also known as AKT) signalling pathway, which results in phosphorylation and inhibition of the sensitizer protein B-cell lymphoma 2 (BCL-2)-associated death promoter (BAD) [44]. Here, AKT1 is linked to idiopathic pulmonary fibrosis.