Apolipoprotein C2 (APOC2) forms a complex with the enzyme lipoprotein lipase (LPL) to facilitate the hydrolysis of TG, thereby generating FFAs for cellular metabolism.[33, 34] LPL is markedly upregulated in NSCLC, which significantly reduces the survival time of these patients.[35] Extracellular FFA levels were not induced when APOC2 was knocked down, and were increased after APOC2 overexpression even when oxamate was used to inhibit lactate levels (Figure 3C). Here, APOC2 is linked to non-small cell lung carcinoma.