Scientists at the Cleveland Clinic Foundation have developed small-molecule inhibitors that inhibited the bacterial enzyme chain responsible for processing choline into trimethylamine-N-oxide (TMAO).

Stanford University scientists have shown that homeostatic plasticity was disrupted in fragile X syndrome (FXS) through effects on retinoic acid (RA) signaling. The fragile X mental retardation 1 (FMR1) gene that is mutated in FXS codes for an RNA binding protein with multiple interaction partners.

The gene STK11 encodes the tumor suppressor liver kinase B1 (LKB1), and STK11 mutations promote Peutz–Jeghers syndrome (PJS), a cancer predisposition syndrome. Individuals with PJS are prone to developing gastrointestinal polyps, which can lead to gastrointestinal (GI) tumors. Researchers from the Van Andel Research Institute and the Canadian McGill University have shown that STK11 mutations led to increased inflammation, and that targeting the inflammation could improve outcomes in mouse models of PJS. 

Researchers from the University of Toronto's Sunnybrook Health Sciences Centre have demonstrated that they could safely and reversibly open the blood-brain barrier (BBB) by using MRI-guided ultrasound combined with microbubbles.

Researchers from the Japanese Kobe and Kyoto Universities have demonstrated that in mice, innate immune activation via Toll-like receptors (TLRs) was necessary for social defeat stress to translate into depressive behaviors.

Scientists from the Georgia Institute of Technology have developed polymeric microparticles that could be loaded with therapeutic bacteriophages, and delivered to the lungs via inhalation. Treatment with the phages protected both regular mice and mouse models of cystic fibrosis from otherwise lethal infections with Pseudomonas aeruginosa.

Using genome editing in liver cells, researchers from the University of Pennsylvania have lowered the levels of LDL "bad" cholesterol in monkeys by up to 60 percent.