Third, this reduced post-translational modification impairs Hsp47's ability to bind to type I pro-collagen molecules in the tumor ECM and transport them to the Golgi apparatus, leading to the accumulation of immature type I pro-collagen within the ER, which subsequently inhibits the biosynthesis of collagen I. These coordinated mechanisms ultimately lead to a significant inhibition of CRC growth. The gene discussed is SERPINH1; the disease is neoplasm.