Anti-targets are proteins that cause problems when inhibited along with an intended target and our novel chemical strategy affords unprecedented selectivity in the context of FLT3 vs. KIT inhibition for treatment of a devastating blood cancer.

The secreted sugar-binding protein galectin-8 causes osteoblasts to secrete factors that promote the differentiation of bone marrow cells into osteoclasts; targeting this protein could therefore potentially help treat diseases associated with excessive bone loss.

Orphan nuclear receptor Nur77 protects bone by enabling a timely termination of osteoclast differentiation.

Mice that overexpress VEGF-C in bone display a phenotype that resembles Gorham-Stout disease.

Rgs12 protein is a novel regulator of the Nrf2 protein by facilitating the proteasomal degradation of the transcription factor during osteoclast differentiation.

Cartilage and bone tumors arise from chondrocyte or osteoblast progenitors but not differentiated cells or multipotent mesenchymal stem cells (MSCs) via the IHH-Wnt/β-Catenin pathway.

Mechanical stimuli activate Piezo1 in osteoblast lineage cells and thereby promote bone formation in part via Wnt1.

Mechanosensitive channels Piezo1/2 are required for osteoblast differentiation from progenitors by sensing fluid sheer stress and matrix rigidity and regulating NFATc1, YAP1 and ß-catenin activities through Ca²⁺ stimulated phosphatase calcineurin.

A high-phytate-low Ca²⁺ diet causes crystal nephropathies, renal phosphate wasting, and bone disease in rats, whereas high Ca²⁺ intake ameliorates the detrimental effects of a high-phytate diet.

Site-specific modification of NEMO facilitates RANKL signal specificity in myeloid progenitors and serves as a potential target to modulate inflammatory osteolysis through ISG15-dependent autophagy.