Despite the different mechanisms implicated in cell toxicity between BRICHOS and non-BRICHOS mutations of SFTPC, similar gene expression changes in the same pathways were observed in the patient-derived AEC, suggesting that such common early epithelial transcriptomic changes may predict the future development of interstitial pneumonia and comparative analysis of alveolar organoids generated from multiple patient-derived iPSC with various SFTPC mutations would lead to elucidate the pathogenesis of ILD. This evidence concerns the gene SFTPC and interstitial lung disease.