First, from a functional perspective, the IGF1/PI3K/AKT axis is a well-recognized driver of EMT in IPF: binding of IGF1 to its receptor activates PI3K, leading to AKT phosphorylation and subsequent upregulation of EMT transcription factors, which directly downregulate the epithelial marker E-cadherin and upregulate the mesenchymal markers Vimentin and α-SMA [33,34]. Here, VIM is linked to idiopathic pulmonary fibrosis.