More recently, BRAF inhibitors induced β-catenin accumulation in CAF, stimulated the secretion of the downstream effector POSTN of β-catenin signaling, and finally activated ERK signaling to allow melanoma cells to continue proliferating in the presence of BRAFi and MEKi, suggesting that explicitly targeting POSTN may be one of the promising options [432–434]. The gene discussed is POSTN; the disease is melanoma.