BRAF and melanoma: To disrupt collagen architecture, we employed two pharmacological inhibitors: 3,4‐dihydroxybenzoic acid (DHB), which inhibits collagen prolyl 4‐hydroxylase and thereby prevents collagen triple helix formation, and β‐aminopropionitrile (BAPN), a lysyl oxidase inhibitor that blocks collagen crosslinking.[19, 20, 21, 22] Using our established melanoma model, we initiated treatment with DHB or BAPN on day 10 of BRAF/MEKi therapy, coinciding with the onset of residual disease, while maintaining continuous BRAF/MEKi administration (Figure4A).