In the case of TRP-targeted drug discovery for ME/CFS, patch-clamp electrophysiological techniques have revealed a potential benefit of low-dose naltrexone (LDN, 3.0–5.0 mg/day), which antagonizes the μ opioid receptor and thus relieves TRPM3 inhibition [14]. The gene discussed is TRPM3; the disease is myalgic encephalomeyelitis/chronic fatigue syndrome.