Treatment with the TRPV1 agonist resiniferatoxin potently induced the phosphorylation of Akt in MM cells, which was almost completely abrogated by addition of the PI3K inhibitor LY294002 (Figure 1B), indicating activation of the PI3K-Akt pathway in MM cells directly via TRPV1. The gene discussed is AKT1; the disease is Miyoshi myopathy.