The ECM, though classically viewed as a structural scaffold, actively shapes cell signaling, immune infiltration, and drug response.[27] Previous studies in melanoma have shown that collagen accumulation in BRAF‐inhibited xenografts promotes resistance through reactivation of MAPK signaling or survival pathways such as DDR1/2 and integrin β1/FAK.[15, 16, 28, 29, 30, 31] In those studies, the outcome of changes to the ECM was examined primarily through the lens of melanoma cell–intrinsic adaptations. Here, BRAF is linked to melanoma.