CD8A and neoplasm: Indeed, previous studies have demonstrated that MC38 tumors are far less susceptible to Treg inhibition than other tumor models, indicating that resistance to immunotherapy is provided by alternative cellular mechanisms.40 41 Furthermore, a study by Gyori and colleagues demonstrated that MC38 tumors were non-responsive to the PI3Kδ inhibitor, Idelalisib, and could only be controlled when therapies that targeted both Tregs and tumor-associated macrophages were employed together.42 It appears that an alteration in the CD8:Treg ratio is a requisite of successful PI3Kδ inhibition.