Sympathetic-sensory nerve cross-talk drives tumor progression and neuropathic pain in oral cancer, implicating peripheral neuroplasticity as a target.

A transient, postoperative window of blood-brain barrier permeability enables repurposing of clinically used liposomal nanoparticles for glioblastoma.

In the Research Resource “Pharmacogenomic landscape of head and neck squamous cell carcinoma informs precision oncology therapy” by Z. Gu et al., formatting errors were present in data file S1, including inconsistent numbers of decimal places across values in the raw data for fig. S2 and a duplicated header label of Fig. 6H. Data file S1 has now been corrected with consistent formatting of all numerical values. The original values themselves were correct, and no other analyses, figures, or conclusions were affected.

Intravesically delivered engineered bacteria promote PD-1 blockade efficacy in aggressive murine models of bladder cancer.

Anti-CD20 B cell depletion augments mucosal regulatory IgA B cell trafficking in multiple sclerosis.

Sequential kidney biopsies reveal that SGLT2 inhibitors reverse metabolic and inflammatory kidney dysregulation in youth with T1D.

Complement C1q and C3 potentiate neutralization activity of anti-S2 antibodies against SARS-CoV-2 variants via the Fc region.

Evaluation of infants’ spontaneous motor activity with at-home wearables helps construct detailed growth charts of early gross motor development.

Sickle cell disease–induced hematopoietic stem cell senescence and loss of function are reversed in SCD mice by treatments targeting senescence.

Antagonizing the VIP-VIPR pathway results in phenotypically and functionally superior CAR T cells that boost endogenous immunity.

IFN-γ is dispensable for mediating protection of mice from pneumonic plague after vaccination.

The authors of the Research Article “Phase separation–based HTS identifies cobimetinib as a YAP-TEAD inhibitor that suppresses hyperactivated YAP-induced cancer progression” by R. Yang et al. present one correction and two clarifications in the Supplementary Materials. In fig. S5, the values for 0.37 μM GNE-7883 in NCI-H2052 and NCI-H2373 cells were identical to those for 0.04 μM because of a copy-paste error. The authors retrieved the original data and corrected fig. S5 in the Supplementary Materials PDF and the data in data file S1. Some controls or samples were processed in the same experimental batch to minimize batch-to-batch variability and conserve samples. However, the data were presented in different figure panels for addressing distinct biological questions. To avoid misinterpretation, notations indicating concurrent samples have been added to data file S1 as follows: asterisk (*) for Fig. 4, N and O; asterisk (*) and hash tag (#) for Figs. 5A and 6A; and color marks for fig. S3A. In addition, the full-precision decimal values, raw measurements, and the calculation formula for fig. S21D are provided in data file S1 to avoid misinterpretation caused by rounding. The correction and clarifications do not affect the interpretation of the experiments or conclusions of the study.

PTEN drives the pathogenesis of nonhealing venous leg ulcers in humans, and its inhibition accelerates wound healing in mice.

Autoantigen-specific Tr1 cells repair autoimmune demyelination by delivering amphiregulin to the oligodendrocyte epidermal growth factor receptor.

Omics-guided discovery identified a protein kinase A modulator that reduced motor symptoms and l-dopa–induced dyskinesia in Parkinson’s disease models.

A culturable nasopharyngeal bacterial catalog was built, which reveals mutualism between Fusobacterium and Prevotella that affects tumor therapy response.

Intracortical microstimulation in humans is safe and efficacious for up to 10 years.

CD4+ T cells in MS preferentially recognize EBV viral particles rather than latent antigens, and responses are reduced by B cell–targeting therapies.

Mitochondrial uncoupling limits atheroprogression by improving insulin sensitivity, lowering triglycerides, and suppressing inflammasome activation.

Kidney-infiltrating CD8+ T cells in human lupus nephritis are activated via local cytokines and have the capacity to amplify local inflammation.