The first theory suggested that in the case of BRAF-mutated skin cancers, BRAF inhibitors inhibit MAPK (mitogen-activated protein kinase)-signaling pathways (pERK), causing cell cycle arrest, apoptosis, and inhibiting tumor progression; however, in the case of wild-type BRAF cells, the ERK is activated and causes abnormal cell proliferation, which may lead to SCC development [76,77]. The gene discussed is BRAF; the disease is neoplasm.