Preclinical studies have demonstrated that repressing MYC by targeting BET proteins enhances lymphoma cell vulnerability to PI3K inhibitors through the upregulation of several PI3K pathways genes and increased GSK3β phosphorylation, resulting in increased β-catenin protein abundance [72,73], suggesting that combinatory targeting of PI3K with SRX3305 would further promote MYC degradation by allowing GSK3β-dependent MYC phosphorylation [74] and stabilization of the MYC antagonist, MAD1 [75]. The gene discussed is GSK3B; the disease is lymphoma.