Our findings indicate that the CINNAMcompound may influence the proliferative behavior of tumor cells byaffecting the RAS pathway and/or redox metabolism. However, apparently, the higher responsiveness of A549to CINNAM compared to H1299 seems to be related to the NRF2 signalingpathway. The A549 cell line exhibits aberrantly active NRF2 due toa somatic mutation of the KEAP1 gene at G333C and epigenetic alterationby methylation in the KEAP1 promoter. Further studies will be performed to validate this hypothesis. The gene discussed is KEAP1; the disease is neoplasm.