Resulting efflux through SLAC1 causes membrane depolarization, which activates outward rectifying K+ channels, leading to KCl and water efflux to reduce turgor further and cause stomatal closure. Recent study demonstrated that bicarbonate is a small-molecule activator of SLAC1. Thereby the bicarbonate activates the SLAC1 anion channels. However, the molecular mechanisms that underlie the SLAC1 activation and stomatal CO2 signalling have remained relatively obscure. Some logical questions arise from these new findings. How does the concentration of HCO3– and CO2 activate the SLAC1 to maintain the influx of anions and adjust the pressure in guard cells of stomata? The subcellular location of SLAC1 was experimentally determined in the surface of the guard cell using combined SLAC1 protein and green fluorescent protein. Further experiment examined that the SLAC1 is in the plasma membrane. Therefore, the SLAC1 is a plasma-membrane-localized protein in the guard cells, and participates in the control of anion fluxes across the plasma membrane of guard cells. Usually the reversible conversion of between CO2 and HCO3– is a very slow process without the catalysis by carbonic anhydrases. This is the phenomena of the conversion between CO2 and HCO3– in a uniform solution with constant pH value. The proposed model of SLAC1 channel consists of several regions with different pH values. This is only possible in a micro channel. Just the different pH values elevate the concentration of CO2, and make the conversion between CO2 and 1-Deacetylnimbolinin-B much faster than in uniform macro solution. This is like the case when a drop of hydrochloric acid is put in NaHCO3 solution, the CO2 escapes out quickly. In the cartoon model of AtSLAC1 channel, the top region and bottom region are modeled as the alkaline solutions. However, the two regions are best to be described as the alkaline buffer solutions, because of the alternately distribution of alkaline residues and acidic residues. Carbon dioxide is a key reactant in plant photosynthesis. The continuing rise in of green house gas CO2 in atmosphere is predicted to have diverse and dramatic effects on the productivity of agriculture, plant ecosystems, and global climate. The CO2 conducting mechanism and concentrating mechanism in plant SLAC1 channel, derived in this study based on the structure of AtSLAC1, may provide useful insight into this important research topic. In an ongoing study, we use saliva, an accessible and noninvasive biofluid, for the early detection of diseases, such as Sjo¨gren’s syndrome or pancreatic, breast, and oral cancer. Detecting the differential expression of salivary biomarkers between normal and diseased patients at both the mRNA and protein level allows us to detect specific diseases efficiently. We have shown that a combination of four RNA biomarkers differentiates pancreatic cancer patients from non-cancer subjects, yielding a receiver operating characteristic plot area under the curve value of 1-Tigloyltrichilinin sensitivity and 95.0% specificity. Although these translational and clinical findings provide an innovative breakthrough for the detection of systemic diseases, how distal systemic diseases mediate the presence of disease-indicating salivary biomarkers in the oral cavity remains unclear. The present study demonstrates that interplay between salivary gland cells and tumor-derived exosome-like microvesicles induces in vitro changes in salivary gland cell-derived exosome-like microvesicles. Exosomes are cell-derived vesicles that stably reside in many body fluids, including blood, breast milk, urine, and saliva. Exosomes are formed by the inward budding of multi-vesicular bodies, a component of the endocytic pathway, and consistently manufactured and secreted into the surrounding extracellular matrix and circulation through the fusion of MVBs with the plasma membrane. Due to their novelty, the physiological functions of exosomes have not yet been elucidated.