Among these subgroups, myCAFs (Figure 3E) exhibited high expression of a unique set of collagens and matrix metalloproteinases (MMPs), suggesting their potential role in remodeling the extracellular matrix (ECM) and organizing collagen fibrils.[25] In addition, we noted that myCAFs in HRD tumors also featured high expression of two tyrosine kinase receptors, FGFR1 and PDGFRΒ (Figure 3F,G), which implied the potential therapeutic efficiency of tyrosine kinase inhibitors (TKIs) for HRD patients. Here, FGFR1 is linked to hypoparathyroidism-retardation-dysmorphism syndrome.