Psoriatic arthritis is a complex, immune-mediated inflammatory disease affecting peripheral and axial joints, entheses, skin, and nails. The IL-17 cytokine family, which includes several dimeric isoforms with overlapping and distinct functions, has been implicated in the pathogenesis of psoriatic arthritis. In particular, IL-17A and IL-17F, which share 50% homology and exhibit overlapping proinflammatory activity, can form both homodimers and heterodimers. Increased expression of these cytokines has been observed in the synovial tissue, entheses, and skin of patients with psoriatic arthritis. Secukinumab and ixekizumab, IL-17A inhibitors, have shown efficacy and tolerability in treating psoriatic arthritis. Bimekizumab, a humanized IgG1 monoclonal antibody, selectively inhibits both IL-17A and IL-17F.To effectively reduce inflammation in psoriatic arthritis, both IL-17A and IL-17F need to be neutralized. This suggests that dual inhibition of these cytokines could be an effective treatment approach.