Moreover, in analogy to other types of cancer [18–20], therapy-related resistance based on a treatment-induced shift in KRAS and/or BRAF mutation status could also play a role in explaining the low therapeutic efficacy of anti-EGFR therapy in mCRC by rendering tumor cells initially responsive to anti-EGFR mAbs resistant to this therapeutic regimen [9]. Here, BRAF is linked to neoplasm.