In this study, several lines of evidence confirmed the redundant function between FXR1 and FXR2: 1) both FXR1 and FXR2 can rescue FXR1 shRNA-inhibited cell proliferation (Figure 1D), 2) FXR1 and FXR2 share a significant portion of overlapping binding sites in the genome (Figure 5I, Figure 5—figure supplement 4B–C), and 3) knockout of either protein sensitizes TP53 homozygous deletion-containing cancer cells for the inhibition of the remaining member (Figure 2D, Figure 2—figure supplement 2). The gene discussed is FXR2; the disease is cancer.