The weak correlation between AHK4 and low K signaling may be explained by its dual activity. In the presence of CKs, AHK4 possesses kinase activity and phosphorylates AHPs; however, in the absence of CKs, AHK4 acts as a phosphatase that dephosphorylates AHPs. This finding differs from the regulation of other macronutrients by CKs. AHK3- and/or AHK4-dependent CK signaling was proposed to have dominant roles in the function of nitrate, Reversine phosphate and sulfate transporters. These data suggest that there might be some specificity of CK signaling to each macronutrient signaling pathway and that AHK2 and AHK3 might have major roles in low K signaling. As a common response to K deficiency, ROS is induced in roots, leading to root hair elongation. The investigation of ROS induction in ahk2ahk3 roots further supports the observation that CK signaling is involved in the response to low K. Results shown in Figure 4 indicated that the ROS accumulation was not altered in the ahk2ahk3 mutant by K availability, whereas a significant difference was observed in ROS accumulation in WT either with or without K. Similar to low K-dependent primary root growth, we only observed a slight responsiveness of root hair elongation to low K in the ahk2ahk3 mutant. It is well known that CKs and ABA have antagonistic effects on responses to a number of stresses, including drought and high salinity. Our data, together with previously published results, demonstrate that CKs and ABA also have opposite effects on the response to low K conditions as well. In accordance with their function, CK levels were decreased in WT plants under K-deficient conditions, whereas ABA levels increased.One ab initio study by Covani et al. identified genes with potential roles in periodontitis, some of which have not previously been associated with the disease. However, the protein expression of these genes in periodontitis-affected tissues has not been confirmed. In our study we aimed to identify genes involved in the pathogenesis of periodontitis. Therefore, we further searched through the differentially expressed genes, focusing on the top 50 upregulated genes. Two of these 50 upregulated genes, IRF4 and CCL18, were also detected at the protein level in periodontitis affected-tissues, supporting these genes as novel finds in the pathogenesis of periodontitis. Furthermore, these two selected genes have been reported to be involved in other chronic inflammatory diseases such as RA. The transcription factor, IRF4, has been demonstrated to be involved in T-cell-dependent chronic inflammatory diseases such as IBD. Mudter et al. 2011 reported a correlation between mRNA levels of IRF4 and production of cytokines such as IL-6 and IL-17 in the inflamed colon from patients with IBD, indicating that IRF4 is involved in the regulation of chronic mucosal inflammation. In addition, the gene for CCL18 was upregulated in periodontitis-affected gingival tissues. This chemokine, expressed by macrophages, monocytes and dendritic cells, has been demonstrated to be increased in synovial tissue of RA patients. It has also been suggested that blockage of CCL18 expression by anti-TNF-a antibodies identifies CCL18 as an additional target for anti-TNF-a therapy in patients with RA. Studies are currently ongoing to investigate the expression of candidate genes novel for periodontitis in a larger cohort of patients with periodontitis and healthy controls, to be able to evaluate their impact and to further explore the possible therapeutic targeting of these genes.