And the ALK-independent mechanisms included activation of EGFR, TP53, NRAS-G12D, and MAP3K1 mutations, neurofibromatosis type 2 (NF2) loss-of-function mutations, EMT, and transformation to neuroendocrine carcinoma (105, 110, 114, 122, 123). The gene discussed is NF2; the disease is neuroendocrine carcinoma.