Indeed, in a conditionally activatable Lox-Stop-Lox KrasG12D mouse model [58], loss of LKB1 function resulted in faster tumor development, expanded histological lung cancer spectrum (adeno-, squamous, and large-cell carcinoma) and higher metastasis frequency compared to mice lacking other oncosuppressor genes like p53 or Ink4a/Arf [57]. The gene discussed is CDKN2A; the disease is neoplasm.