Given that both inhibition of autophagy and HIF2α expression contributed to VHL-elicited tumor-suppressing effects, we next treated mouse tumor derived from VHL-deficient 786-O cells with SAR405, a VPS34 inhibitor (Pasquier, 2015), and PT2385, a HIF2α inhibitor, which is currently used for advanced ccRCC patient treatment (Chen et al, 2016; Courtney et al, 2018; Wallace et al, 2016). This evidence concerns the gene EPAS1 and neoplasm.