This can be achieved by normalizing therapy-induced ECM stiffening using therapeutics against TGFβ signaling [91], targeting LOX and LOXL2 collagen cross-linkers [92] or using approved anti-fibrotic drugs such as nintedanib [93], which has shown promising activity in a preclinical model of BRAF mutant melanoma exposed to TT [61]. This evidence concerns the gene LOXL2 and melanoma.