Similar are the cases of other universal oncomiRs—they mostly support oncogenic pathways by either repression of translation or promotion of mRNA degradation of oncosuppressors, e.g., miR-31 downregulates the WNT pathway antagonists and contributes to breast tumorigenesis [228], miR-221 targets DDIT4 transcript, a negative regulator of the mTOR pathway, contributing to liver tumorigenesis [229], miR-155 inhibits C/EBPβ, leading to HK2 overexpression and the metabolic support of cancer cells [230]. This evidence concerns the gene MTOR and cancer.