TGF-β stimulation of tumor cells was shown to increase SHP1 phosphatase activity in an AKT-Smad3-dependent manner, decrease IFNγ-mediated tyrosine phosphorylation of JAK1/2 and STAT1, and inhibit STAT1-dependent immune evasion-associated molecule expression, such as PD-L1, IDO1, herpesvirus entry medium (HVEM), and galectin-9 (Gal-9). This evidence concerns the gene AKT1 and neoplasm.