Several molecular pathways have been identified to mediate the miRNA-34a role in this context, including Notch-1 and Notch-2 pathway suppression, which implicated in self-renewal and colon stem cells differentiation39,40, tumor-initiating cells (cancer stem cells) regulation41,42, and Fos-related antigen-1 (FRA1) targeting23 which plays an essential role in mediating the crosstalk between the oncogenic RAS-ERK and TGFβ signaling networks implied in "epithelial-mesenchymal plasticity" during CRC progression43. The gene discussed is TGFB1; the disease is neoplasm.