On the other hand, in esophageal cancer, increased FGFRL1 expression correlates with disease progression and is directly repressed by miR-107, whereas in small-cell lung cancer FGFRL1 promotes chemoresistance via an ENO1–PI3K/Akt axis, and in pancreatic cancer models exosomal miR-210 from cancer stem cells targets FGFRL1 to drive macrophage M2 polarization and gemcitabine resistance [68,69]. This evidence concerns the gene FGFRL1 and small cell lung carcinoma.