Recent observations in the non-BRAF-mutated B16-F10 melanoma model indicate that inhibition of the DDR2 collagen receptor [82] or CAF-mediated fibrosis by nintedanib [83] improved the antitumor activity of ICB, reinforcing the idea that targeting ECM remodeling is a promising therapeutic approach to enhance immunotherapies in cancer. This evidence concerns the gene BRAF and melanoma.