In an oncogenic KRAS-driven mouse model of lung cancer where inactivation of LKB1 increases lung tumor burden, restoration of LKB1 activated the transcriptional program driven by CEBP (CCAAT enhancer binding protein), reinstated alveolar type II cell-like differentiation and consequently impeded proliferation and growth of lung tumors (Murray et al., 2022). This evidence concerns the gene KRAS and lung cancer.