Recently, it has been also shown that efficacy of the PI3Kδ/γ inhibitor duvelisib in combination with the Bcl-2 inhibitor venetoclax in Richter Syndrome (RS) patient-derived xenograft models, is due to GSK3β activation by PI3K inhibition which leads to c-myc and Mcl-1 degradation, making RS cells more sensitive to Bcl-2 inhibition [61]. Here, MCL1 is linked to Richter syndrome.