Most preclinical studies investigating BRAF/MEKi resistance, particularly those exploring ECM alterations as a mechanism, have relied on immune‐deficient models, which cannot capture the complex interplay between tumor cells, the extracellular matrix, and host immunity.[15, 16, 30] Here, using an immune‐competent mouse model of BRAF‐mutant melanoma, we defined dynamic changes in ECM gene expression across two critical treatment phases: active regression and therapy‐tolerant residual disease. Here, BRAF is linked to neoplasm.