Intrigued, or rather stimulated, by the unjustified negligence of researchers in capitalizing on the benefits of dual HDAC6–HSP90 inhibition as a promising ocular therapeutic strategy, we believed that the task of developing therapeutics for wet AMD should involve the construction of chemical tools that can simultaneously inhibit HDAC enzymes and HSP90 chaperone proteins. The gene discussed is HSP90AA1; the disease is wet macular degeneration.