Evidence gathered over the last years indicates that tumor pathologies, including neuroendocrine tumors (NETs) share as a common feature the altered expression of functionally and pathologically relevant splicing variants of diverse molecules, from membrane receptors to key signaling enzymes (DLK1, GHRHR, IGF1R, EGFR, CSH2, or PTEN) [35,36,37,38]. The gene discussed is CSH2; the disease is neoplasm.