To test this hypothesis, we first treated age-matched leukemia-stage Pten-null T-ALL mice with DB1976 (Figure 11—figure supplement 1A–B), a compound known to specifically disrupt the interactions between SPI1 and its targets (Antony-Debré et al., 2017; Munde et al., 2014; Stephens et al., 2016). The gene discussed is PTEN; the disease is leukemia.