BRAF and colorectal carcinoma: The remaining 25–30% of CRC arise from sessile serrated lesions (SSLs) through the SSL-to-carcinoma pathways (Figure 2B), associated with mutations in the proto-oncogene BRAF (v-raf murine sarcoma viral oncogene homolog B), MSI, and gene promoter hypermethylation (CpG island methylator phenotype) [7,19,28,29].