Tayama et al. reported that 5/6 cases of KRAS and BRAF wild-types were resistant in CRC PDOs, while 6/7 cases with either KRAS or BRAF mutations showed good drug response to SCH772984 (an ERK inhibitor), suggesting that the molecular signature of human original CRC tissues may largely resemble the drug sensitivity in the PDOs but is not completely overlapping [94]. This evidence concerns the gene BRAF and colorectal carcinoma.