Tumor necrosis factor alpha (TNF-alpha) inhibitors have revolutionized the management of rheumatic diseases, including rheumatoid arthritis, psoriatic arthritis (PsA), and ankylosing spondylitis (AS). (1) These agents specifically target and neutralize an important cytokine, TNF-alpha, which plays a crucial role in the inflammatory response. During recent years, TNF-alpha inhibitors, including infliximab, etanercept, and adalimumab, have also been approved for the treatment of moderate to severe plaque psoriasis. Paradoxically, the development or aggravation of psoriatic skin lesions has been reported in patients with rheumatic disease treated with TNF-alpha inhibitors, either as single-case observations or during the course of clinical trials. (2 4) More than half of these patients presented with palmoplantar pustulosis, which often represents a therapeutic challenge. We describe another case of palmoplantar psoriasis induced by infliximab in a patient with AS that was aggravated under ustekinumab therapy, a new biologic agent that targets the p40 subunit common to interleukins 12 and 23 (IL-12 and IL-23).