It can be assumed that in the murine melanoma B16 model, the effect of μ-oligonucleotides is more likely provided through the influence on the individual gene targets of miRNAs (MMP9/miR-21, STAT3/miR-17); however, in the lymphosarcoma RLS40 model, treatment with combinations may cause mRNA and protein functioning alterations for both nodal genes (KRAS/miR-17/miR-155; PTEN/miR-21/miR-17) and individual targets (TIMP3, MMP9 or PDCD4/miR-21, STAT3/miR-17). This evidence concerns the gene KRAS and lymphoma.