[7] The protein encoded by this gene is a member of the cyclin-dependent kinase, (CDK) family, which includes CDK4.

[10] The CDK6 gene is conserved in eukaryotes, including the budding yeast and the nematode Caenorhabditis elegans.

The gene spans 231,706 base pairs and encodes a 326 amino acid protein with a kinase function.

[6] The gene is overexpressed in cancers like lymphoma, leukemia, medulloblastoma and melanoma associated with chromosomal rearrangements.

[10] After binding the Cyclin in the PSTAIRE helix, the protein changes its conformational structure to expose the phosphorylation motif.

[16] The CDK6 complex ensures a point of switch to commit to division responding to external signals, like mitogens and growth factors.

[26] There is evidence that CDK6 associates with the centrosome and controls organized division and cell cycle phases in neuron production.

[32] Likewise, the overexpression of CDK6 is also associated with resistance to hormone therapy using the anti oestrogen Fluvestrant in breast cancer.

[33] Loss of normal cell cycle control is the first step to developing different hallmarks of cancer; alterations of CDK6 can directly or indirectly affect the following hallmarks; disregulated cell cellular energetics, sustaining of proliferative signaling, evading growth suppressors and inducing angiogenesis,[9] for example, deregulation of CDK6 has been shown to be important in lymphoid malignancies by increasing angiogenesis, a hallmark of cancer.

[9] Additionally, CDK6 might be altered through genomic instability, a mechanism of downregulation of tumor suppressor genes; this represents another evolving hallmark of cancer.

The MicroRNA (miR) -124 has successfully controlled cancer progression in an in-vitro setting for medulloblastoma and glioblastoma cells.

[36] Another indirect mechanism for the control of CDK6 expression, is the use of a mutated D-cyclin that binds with high affinity to CDK6, but does not induce its kinase activity.

[36] this mechanism was studied in the development of mammary tumorigenesis in rat cells, however, the clinical effects have not yet been shown in human patients.