Interestingly, it has been found that accumulation of FN-EDA in systemic sclerosis-associated interstitial lung disease (Ssc-ILD) fibroblasts is not based on increased transcription but on reduced turnover due to reduced ubiquitination,280 highlighting again that the matrix is not an inert deposition of proteins but a highly dynamic entity. This evidence concerns the gene FN1 and interstitial lung disease.