LPL and non-small cell lung carcinoma: 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).