Comparing solid and acinar samples using gene set variation analyses (GSVA) [34] revealed that hallmarks associated with aggressiveness and metabolic activity, such as G2M checkpoint, angiogenesis, epithelial-mesenchymal transition (EMT), MYC targets V1 and PI3K/AKT/mTOR signaling, were up-regulated in tumor cells from solid samples (Fig. 1A, Additional file 2: Table S2), which was consistent with a more aggressive histopathological phenotype of solid LUADs. The gene discussed is AKT1; the disease is neoplasm.