Negative results of yet another IL-1 inhibitor in the treatment of knee osteoarthritis add to a pool of data indicating that this strategy does not reduce pain or inflammation and is thereby a dead end. Should we therefore shelve further plans to test or use this therapeutic strategy?

Mutations in MYBPC3 cause increased cardiac contractility, reduced relaxation and excessive energy consumption characteristic of hypertrophic cardiomyopathy by disrupting normal myosin conformations. These abnormalities can be corrected by pharmacological targeting of myosin function.