HDACi treatment led to increased MIC A/B expression on uninfected cells with a greater increase with HIV-1 infection (Fig 6E), although there was no difference in ULBP1 or 2 levels with or without HDACi treatment (Fig 6F and 6G respectively) suggesting MIC A/B levels could explain the preferential killing of infected cells through the NKG2D pathway. The gene discussed is ULBP1; the disease is HIV-1 infection.