Similar to other studies finding an accumulation of collagen I in the TME of various cancer types, we found upregulation of col1a1b and col1a2 in CAFs relative to normal fibroblasts, indicating increased collagen I deposition.59,60 The precise mechanism of how different subclasses of CAFs regulate UM differentiation state and propensity to metastasize through ECM remodeling is still to be defined. The gene discussed is COL1A2; the disease is cancer.