Although the 3D model employed here lacks immune cells, we nevertheless found an increased expression of COL4A1, COL4A2, COL6A1, LAMA1, and LAMA2 and other ECM proteins that are commonly associated with a fibrotic phenotype, suggesting the existence of an immune cell-independent pathway underlying fibrosis in Duchenne muscular dystrophy [24, 44]. This evidence concerns the gene COL6A1 and Duchenne muscular dystrophy.