To answer the question about the mechanism by which DHA is able to kill cancer cells while sparing normal cells, Yun et al. [91] conducted the study reporting that cultured human colorectal cancer cells with KRAS (Kirsten rat sarcoma viral oncogene) or BRAF (v-raf murine sarcoma viral oncogene homolog B) mutations were selectively killed when exposed to high concentrations of vitamin C, and that effect resulted from an increased DHA uptake via the GLUT1 glucose transporter. Here, BRAF is linked to colorectal cancer.