CPT1A and neoplasm: However, whereas the combination of Cpt1a ablation and LCKD significantly inhibited tumor growth and enhanced survival (Fig. 6d–f), Cpt1a-deficient tumors on the MCKD grew at a comparable rate to those on normal chow (Supplementary Fig. 11h, i), consistent with the ability of MCFAs to partially rescue the effects of glucose starvation on proliferation and metabolism in vitro.