TNF and rheumatoid arthritis: Beyond direct tissue damage, RA-FLSs engage in inflammatory signaling by producing essential chemokines and cytokines, including TNF and IL-7, fostering the migration, activation, and survival of T and B cells, aggravating oxidative stress through excess ROS production, and expressing RANKL, a key cytokine mediator of osteoclast differentiation and bone resorption [136–138].