Therefore, the critical role of the tranylcypromine-based KDM1A inhibitors in the treatment of AML [45,48] and SCLC [47] are presumably not only due to the inhibition of demethylation activity, but rather to the disruption of protein–protein interactions between KDM1A and interacted transcription factors. The gene discussed is KDM1A; the disease is small cell lung carcinoma.