The KD improves the efficacy of anti-PI3K treatment and drug resistance by decreasing hyperglycemia and reducing the insulin-secretory response, and these effects correlated with reduced intratumoral mTORC1 signaling.241 In a mouse model of melanoma, acceleration of proliferation in BRAF V600E-mutated melanoma cells after the KD treatment was observed because of the selectively increased activation of BRAF V600E-mutant-dependent MEK1 signaling by the KB acetoacetate. The gene discussed is BRAF; the disease is melanoma.