“…In January 2021, Shah et al reviewed granulomatous cutaneous drug eruptions and identified a number of iatrogenic causes of GA: allopurinol, amlodipine, anti-TNFα agents (infliximab, adalimumab, etanercept, and thalidomide), botulinum toxin, dabrafenib, desensitization injections, immune checkpoint inhibitors, intranasal calcitonin, gold, immunizations (hepatitis B and anti-tetanus vaccination), levetiracetam, paroxetine, pegylated IFNα, secukinumab, tocilizumab, topiramate, and vemurafenib [ 49 ]. More recently, acetazolamide [ 50 ], apremilast [ 51 ], ixekizumab [ 52 ], mesotherapy [ 53 ], phototherapy [ 54 ], and measles, mumps, and rubella (MMR) [ 55 ], pneumococcal [ 56 ], and VZV [ 57 ] immunizations have also been implicated in instigating GA. The pathogenesis of drug-induced GA is not easily understood, and the induction of GA by anti-TNFα agents and apremilast in particular is paradoxical, as both TNFα inhibitors and apremilast have also been reported as effective therapies for GA. Instigation of GA by IL-17 inhibitors (ixekizumab and secukinumab) is also intriguing, as Min et al reported hyperactivation of the Th17 axis in GA. We attempt to explain these paradoxical observations in Sect.…”