In another study IL-17 adenoviral overexpression in the knee joint of type II collagen-immunized mice (a murine model of rheumatoid arthritis) promoted osteoclastic bone erosions in cortical, subchondral, and trabecular bone along with expression of RANKL and its receptor RANK in the synovial infiltrate and at sites of focal bone erosions. Here, IL17A is linked to rheumatoid arthritis.