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The majority of trials possess at least one characteristic that may compromise their ability to guide clinical practice.

SF3B1 mutation in myelodysplastic syndromes and acute myeloid leukemia lead to oncogenic long isoforms of IRAK4 that are therapeutically targetable.

Genetic and biochemical analyses uncover a dichotomy of ERK pathway functions in osteoblasts, whereby ERK activation promotes the early differentiation of osteoblast precursors, but inhibits the subsequent differentiation of committed osteoblasts via mTOR-mediated regulation of mitochondrial function and SGK1.

IL-33 plays an important role in the initiation of labor by leading to stress of the ER via an influx of calcium ions in human uterine smooth muscle cells.

Experiments in genetically altered mice reveal that microglia play an important role in the neurological damage associated with neuro-nopathic Gaucher disease.

In neurodegeneration of Gaucher disease, glucosylceramides trigger neuroinflammation via attrition of homeostatic microglia and transition to lipid-laden damage-associated microglia concurrently with infiltration of diverse immune cells including activated NK cells and CCR2⁺ macrophages, ameliorated by substrate reduction therapy.

Lack of cardiac MKK6 results in premature death with the development of heart hypertrophy and cardiac dysfunction in aging.

Under metabolic syndrome, joint subchondral preosteoclasts acquire a senescence-associated secretome, which causes a rapid structural alteration of subchondral bone and contributes to the development of osteoarthritis.

A mathematical model of osteoporosis explains why the sequence of osteoporosis medications matters for short-term and long-term treatment success.

Multiple -omics approaches have provided valuable insight into the pathobiology of pediatric acute respiratory distress syndrome, and novel unbiased techniques hold promise for future discoveries.