5‐Aza decreases the growth and increases the apoptosis of CACO2 cells by relieving the transcriptional limitation of RASSF1A.37 NALP1 can be restored by 5‐Aza to restrict CRC proliferation.38 Ultimately, 5‐Aza stimulates p53‐dependent tumor cell senescence and induces DNA double‐strand breaks.39 Furthermore, aberrant expression of miRNAs in CRC is frequently due to the inappropriate enrichment of epigenetic alterations, including DNA methylation and histone modification.25 Based on these clues, we attempted to build the connection between miR‐487b and this small‐molecule compound in CRC. This evidence concerns the gene TP53 and neoplasm.