Several recent reports have suggested that the primary mechanism of action of LSD1 inhibitors in both AML and SCLC occurs not only through catalytic inhibition of LSD1 enzymatic function but also through inhibition of the interaction of LSD1 with SNAG domain transcriptional factors such as INSM and GFI1B [14, 15]. This evidence concerns the gene GFI1B and small cell lung carcinoma.