AKR1B10 and colorectal carcinoma: Conversely, pharmacological inhibition of PP2A with LB-100 at subinhibitory concentrations robustly reversed c-Myc signaling in control groups, with less pronounced effects in shAKR1B10 CRC cells, underscoring PP2A’s role in regulating c-Myc–driven oncogenic plasticity, particularly under AKR1B10-deficient conditions (fig.