Previous research has demonstrated that elevated NH\({}_{4}\)+ levels lead to a reduction in endogenous free IAA content, while the application of low concentrations of exogenous IAA can mitigate NH\({}_{4}\)+ toxicity [9]. Our recent studies indicate that elevated NH\({}_{4}\)+ diminishes free IAA content by enhancing IAA conjugation rather than by inhibiting IAA biosynthesis. Additionally, the transcription factor AtWRKY46 plays a pivotal role, as it directly suppresses the transcription of IAA-conjugating genes [10]. In addition, exogenous BR treatment significantly suppresses AtPIN2 expression and the nuclear auxin signal under high NH\({}_{4}\)+ stress, indicating that auxin operates downstream of the BR signaling pathway in response to elevated NH\({}_{4}\)+ stress [9]. Beyond IAA and BR, ABA is required for protecting chloroplast and root growth under high NH\({}_{4}\)+ stress [11]. Our recent study shows that high NH\({}_{4}\)+ induces ABA biosynthesis and activates the 'OsSAPK9-OsbZIP20' module, which in turn augments reactive oxygen species (ROS) scavengers and bolsters NH\({}_{4}\)+ assimilation, thereby minimizing ROS and free NH\({}_{4}\)+ accumulation in rice roots [11]. Intriguingly, the ABA signaling elicited by high NH\({}_{4}\)+ levels can also disrupt the interaction between AtAB11 and AtCIPK23 by inactivating AtAB11. As a consequence, the liberated AtCIPK23 is then able to further phosphorylate and inhibit AtAMTs in Arabidopsis [12]. (iv) How does NH\({}_{4}\)+ stress induce a burst of ROS? High-NH\({}_{4}\)+-triggered ROS accumulation has been reported in a previous study; however, the mechanisms underlying the NH\({}_{4}\)+-induced ROS burst remain unclear [13]. Interestingly, two recent studies have proposed that iron (Fe) accumulation might be the primary driver of the NH\({}_{4}\)+-induced ROS burst. When compared to NO\({}_{3}\)-, NH\({}_{4}\)+ induces greater Fe accumulation in the apoplast of the phloem, resulting in a ROS burst. This process appears to involve a cell wall-localized ferroxiidase known as LPR2. Both the knockout of _AtLPR2_ or reduction in Fe supplementation can significantly enhance root growth tolerance to high NH\({}_{4}\)+ stress [14]. Moreover, the acidification of the apoplast, caused by NH\({}_{4}\)+ uptake, results in Fe precipitation in the elongation and differentiation zones of the root tip, which, in turn, induces hydrogen peroxide (H\({}_{2}\)O\({}_{2}\)) accumulation and NH\({}_{4}\)+ toxicity. The knockout of _AtPDX1.1_, an enzyme involved in vitamin B6 biosynthesis, or application of exogenous vitamin B6 could quench ROS and partially rescue root growth under NH\({}_{4}\)+ stress [15]. (v) How do roots regulate NH\({}_{4}\)+/H+ efflux in response to NH\({}_{4}\)+ uptake? The capacity of NO\({}_{3}\)- to mitigate NH\({}_{4}\)+ toxicity has been documented in many species; however, the underlying molecular mechanism remains elusive. Earlier investigations have demonstrated that NH\({}_{4}\)+ uptake results in rhizosphere acidification, whereas NO\({}_{3}\)-uptake leads to its alkalinization [16; 17]. Thus, it is worth exploring whether NO\({}_{3}\)- counteracts the rhizosphere acidification instigated by NH\({}_{4}\)+ absorption and subsequently mitigates NH\({}_{4}\)+ toxicity. Recently, a team from China found that AtsLAH3 (a NO\({}_{3}\)-efflux channel) interacts with AtNRT1.1 (a NO\({}_{3}\)-/H+ symporter) to form a 'transporter-channel' complex to manipulate NH\({}_{4}\)+ influx, NO\({}_{3}\)- influx/efflux, and H+ influx through the membrane [18; 19]. Consequently, the AtsLAH3/ANRT1.1 complex enhances tolerance against NH\({}_{4}\)+ uptake-induced rhizosphere acidification. Beyond the rhizosphere, futile NH\({}_{4}\)+ efflux, triggered by NH\({}_{4}\)+ absorption, is also a predominant factor contributing to NH\({}_{4}\)+ toxicity [10].