SCLC tumors show recurrent somatic alterations in proteins related to cytoskeleton formation or cell–cell and cell–matrix interactions, such as SLIT2 (Slit Guidance Ligand 2) and mutagenic alterations in kinase receptors, like the inactivation of EPHA7 (EPH Receptor A7) and/or the amplification of FGFR (Fibroblast Growth Factor Receptor) and MET [15]. The gene discussed is MET; the disease is small cell lung carcinoma.