In different lung cancer (LC) cellular models (NCI-H460, NCI-H460-LNM35, NCI-H1975, and HCC15), ANGPTL2 is responsible for an increase in GLUT3 expression (and an increase in glycolytic flux) via an integrin α5β1/ERK-dependent pathway impinging on TGFβ and its downstream factor ZEB1, concurrently with the execution of the EMT (Figure 3) [172].ANGPTL2 → integrin α5β1→ERK ⇒ TGFβ ↑ ⇒ ZEB1 ↑ ⇒ (GLUT3 ↑ & EMT). This evidence concerns the gene TGFB1 and laryngotracheoesophageal cleft.