34 discovered that the expression level of miR‐26a in EAC tissues was lower than that in non‐tumour mucosa, and miR‐26a expression was much lower in metastatic lymph nodes than in primary EAC tumours. Down‐regulation of miR‐26a leads to cell cycle arrest but it has little impact on invasion, migration and apoptosis 34. MiR‐26a suppression is favourable for the subsequent metastasis of EAC cells as well as acquisition of anoikis resistance by affecting the Rb1/E2F1 pathway 34. The gene discussed is E2F1; the disease is neoplasm.