Furthermore, Khan et al1139 reported on the role of TRPML1 in cooperation with the big-conductance Ca2+ activated K+ channel (BK) in HIV infection and proposed that TRPML1/BK coactivation leads to an enhanced acidification of endolysosomes, resulting in an increased degradation of Tat protein, which facilitates HIV replication. The gene discussed is KNG1; the disease is HIV infectious disease.