The concept that a targeted agent that blocks a pro-oncogenic mechanism in tumor cell has the potential to activate cell proliferation in a distinct tissue is well-known, not only in patients treated with sorafenib who develop skin cancer, but more frequently with BRAF inhibitors used in melanoma, such as vemurafenib, dabrafenib and encorafenib [22–24]. Here, BRAF is linked to skin neoplasm.