MicroRNA are ubiquitous in higher eukaryotes, and show varying patterns of expression in specific cell types.

[4] MiR-19 has been identified in a diverse range of vertebrate animals including green anole (Anolis carolinensis),[5] primates (gorilla, human, ...),[6][7] cattle (Bos taurus),[8] dog (Canis familiaris),[9] Chinese hamster (Cricetulus griseus),[10] zebrafish (Danio rerio),[11] horse (Equus caballus),[12] Takifugu rubripes,[11] Tetraodon nigroviridis,[11] chicken (Gallus gallus),[13][14] gray short-tailed opossum (Monodelphis domestica),[15] platypus (Ornithorhynchus anatinus),[16] Japanese medaka (Oryzias latipes),[17] African clawed frog (Xenopus laevis),[18] Tasmanian devil (Sarcophilus harrisii),[19] pig (Sus scrofa)[20] and zebra finch (Taeniopygia guttata).

These microRNA are considered as oncogenes which improve proliferation, inhibits apoptosis and induce tumor angiogenesis.

[28][29][30] This pathway is activated through PTEN loss and can contribute to reduce sensitivity to chemotherapy and (in T-ALL) may impact the effectiveness of therapeutic gamma-secretase inhibitors.

Baraniskin and al. study show that miR-21, miR-19, and miR-92a levels in cerebrospinal fluid (CSF) seems to be good biomarkers to diagnose a Primary central nervous system lymphoma (PCNSL).

[31][32] Mu and al. demonstrated that the expression of endogenous miR-17-92 is required to suppress apoptosis in Myc-driven B-cell lymphomas.

A 52-nucleotide-long sequence of the rhoB 3'-UTR spanning bases 818–870, containing the miR-19 and the HuR binding site was sufficient for UV regulation.

The mouse retinal development need miR-17-92 over-expression with Rb and p107 deletion, but it occurred frequent emergence of retinoblastoma and metastasis to the brain.

Here, the cluster oncogenic function is not mediated by a miR-19/PTEN axis toward apoptosis suppression like in lymphoma or in leukemia models.

[35] Scientists observed that the loss of function of the miR-17-92 cluster is induced in smaller embryos and postnatal deaths.

Moreover, transgenic expression of these miRNAs specifically in lung epithelium results in severe developmental defects with enhanced proliferation and inhibition of differentiation of epithelial cells.

Even though this cluster regulates vascular integrity and angiogenesis, none of each members has a significant impact on the endothelial differentiation of pluripotent stem cells.

The main action of miR-19 seems to inhibit protein translation of the tissue factor gene in less invasive breast cancer cells.