BRAF, short for B-Raf proto-oncogene, encodes a cytoplasmic serine/threonine kinase. It plays a key role in regulating the mitogen-activated protein kinase (MAPK) signal transduction pathway, which is crucial for cellular physiological activities such as proliferation, differentiation, apoptosis, and senescence [3,4].

BRAF is frequently mutated in several cancers. In melanoma, it is one of the most frequently mutated oncogenes, with around 40-50% of melanomas having BRAF mutations, mostly at codon 600 (notably V600E), leading to constitutive activation of the BRAF/MEK/ERK (MAPK) pathway [1,5]. In colorectal cancer (CRC), about 10% of patients have BRAF mutations, which are associated with poor response to chemotherapy and prognosis [2]. In non-small cell lung cancer (NSCLC), BRAF mutations occur in 1%-2% of adenocarcinoma cases, often in never-smokers and women [6]. BRAF-targeted therapies like BRAF inhibitors have shown promise in treating BRAF-mutated cancers, but resistance mechanisms frequently develop [1,2,6,7,8].

In conclusion, BRAF is a critical regulator in the MAPK pathway, and its mutations are closely associated with the development and prognosis of multiple cancers. The study of BRAF-mutated models has provided insights into cancer pathogenesis and therapeutic strategies, highlighting the importance of understanding BRAF-related mechanisms for better cancer treatment.