For example, miR-149 was highly expressed in nasopharyngeal carcinoma and promoted malignant progression by suppressing the expression of its target gene, Smad2 [25]; Its oncogenic role was also demonstrated in melanoma in which miR-149 upregulation caused the downregulation of GSK3- and upregulation of Mcl-1, leading to apoptotic resistance [26]. Here, MCL1 is linked to nasopharyngeal carcinoma.