Our previous work [10] identified PI3Kδ inhibition as a promising strategy for glucocorticoid potentiation in B-ALL for two main reasons: (1) small-molecule inhibitors against PI3Kδ are available for clinical use, and (2) PIK3CD expression is restricted to leukocytes, targeting glucocorticoid potentiation to these cells without increasing off-tumor toxicities. The gene discussed is PIK3CD; the disease is neoplasm.