KCNK9 (also named TASK3 or K_2P9.1) is a member of the 2-pore (2P) domain K⁺ channels family that probably assemble as dimers to constitute a functional channel.¹ These channels show little time- or voltage-dependence and are considered to be “leak” or “background” K⁺ channels, thereby generating background currents which help set the membrane resting potential and cell excitation.  

The channels are regulated by diverse physical and chemical stimuli including temperature, pH, mechanical stretch, inhalation anesthetics, etc.² The physiological role of the K_2P channels is not yet clear, though they were proposed to participate in breathing, aldosterone secretion and anesthetic-mediated neuronal activity.

In human, expression of KCNK9 is restricted in brain and its expression overlaps with the structurally related KCNK3 (TASK1, K_2P3.1) channel. In rat, it is more widely expressed in other tissues as well as in brain.  

Unexpectedly, KCNK9 was found to be over-expressed between 5 to 100-fold in 44% of breast cancer tumors tested.  
Transfection and over-expression of KCNK9 in cell lines promotes tumor growth and confers resistance to hypoxia and serum deprivation.³ Recently, KCNK9 was found to play an important role in K⁺-dependent apoptosis of cerebellar granules.⁴