[42], [43] Our study revealed that MCL-1 was overexpressed in breast cancer cells and ectopic restoration of miR-26a significantly decreased MCL-1 protein expression. In addition, miR-26a expression level was much higher in breast cancer tissues of MCL-1 negative group patients. Furthermore, functional studies by knockdown of MCL-1 phenocopied overexpression of miR-26a in breast cancer cells, resulting in cell growth and proliferation suppression in vitro, suggesting that the growth inhibitory effect of miR-26a was partly implemented by means of repressing MCL-1 expression. The gene discussed is MCL1; the disease is breast carcinoma.