found that transient inhibition of PI3Kδ by the PI3Kδ-selective inhibitor IC87114 or the clinically approved idelalisib (CAL-101) prior to intravenous delivery of a tumor-tropic VACV could inhibit viral attachment to, but not internalization by, systemic macrophages through perturbation of signaling pathways involving RhoA/ROCK, AKT, and Rac, thus potentiating intravenous delivery of oncolytic VACVs to tumors (115). This evidence concerns the gene AKT1 and neoplasm.