As the tumor grows, the volume of ECM progressively increases, which leads to the transmission of signals from ECM to the cell through integrins and mediators, the inclusion of p38MAPK/ERK signaling cascades, and conserved signaling pathways, which coordinately regulate diverse cellular activities and is accompanied by impaired expression of the TGF-β (transforming growth factor β), ACVR1 (activin A receptor, type I), PDGF (platelet-derived growth factors), and TNF-α (tumor necrosis factor-alpha) genes that regulate the metabolism of steroid hormones estrogen and progesterone. This evidence concerns the gene ACVR1 and neoplasm.