Other members of the FGF superfamily are critical for normal development of the auditory system in humans and animal models, kidney and inner ear development rely on shared molecular mechanisms and genetic pathways and both organs are susceptible to toxicity from aminoglycoside antibiotics and loop diuretics. Additionally, deficiency in klotho, a critical co-factor for FGF23 mediated signaling, results in hearing loss. Alpha-KL is a single-pass transmembrane protein that increases FGF receptor affinity for FGF23 and decreases affinity to other FGFs. KL expression has been Ginsenoside-F5 reported in several cochlear cell types, but the sensory epithelia of Kl2/2 mice appear normal. Overall, this divergence of Fgf23 and Kl phenotypes is made more interesting by recent research which has suggested a calcineurin-mediated FGF23 signaling pathway, and activation of calcineurin has previously been shown to contribute to noise induced hearing loss. Our results raise questions concerning the prevalence of hearing loss among individuals with FGF23 deficiencies. No auditory phenotype has been reported in FGF23-mediated familial tumoral calcinosis, which results from a missense mutation in FGF23. However, diseases with known elevations in serum concentrations of FGF23 co-present with hearing loss. Our findings demonstrate that FGF23 deficiency is sufficient to induce profound sensory impairment in mice. The lack of such an obvious phenotype in humans suggests Sipeimine important differences between species, potentially stemming from robust protection against hypervitaminosis D in humans. Alternatively, a putative auditory phenotype in humans may be less severe, and therefore less studied, than the debilitating systemic phenotypes. Our findings also suggest a potential role for FGF23 in otitis media, a clinically important disease that afflicts 75�C90% of Americans at least once before 3 years of age. Otitis media is estimated to cost the national healthcare system more than $4 billion annually, and in extreme cases can result in long-term speech and learning impairments. Currently, genetic risk factors are poorly understood, but the prevalence of pediatric cases is commonly believed to be related to the ongoing maturation of the Eustachian tube, which undergoes significant development in the first decade of life. It is believed that a FGF23-independent mechanism of phosphate homeostasis must be functioning prior to this age. Our observations support this suggestion as structures which are nearly mature by P10 show very little dysplasia while structures undergoing continued maturation demonstrate more drastic phenotypes. At P10, the ossicles of wildtype mice are still surrounded by mesenchyme, indicating incomplete development, while the remainder of the inner ear space has begun to clear the mesenchymal tissue. In humans with reduced FGF23 activity, familial tumoral calcinosis, hyperphosphatemia may present as early as 21 months old, indicating that FGF23 is important in phosphate handling when most episodes of otitis media develop. Given the potential temporal and mechanistic overlap of initiation of FGF23 activity and Eustachian tube development, this work suggests a possible role for FGF23 in the genetic predisposition to otitis media, a link that warrants further investigation. Meanwhile, quinclorac is highly stable, and degradation of quinclorac in nature is very slow. The quinclorac residues are phytotoxic to many crops and vegetables, which has become one of the major problems in their rotation with rice.