Furthermore, Vorinostat inhibited PI3K (p110α), p-PI3K p55, and p-Akt protein expression and upregulated major histocompatibility class I-related chain A (MICA) expression in vitro and in vivo, which promoted natural killer (NK) cell-mediated cervical cancer cell lysis. The gene discussed is AKT1; the disease is cervical carcinoma.