APDS mostly results from gain‐of‐function mutations in the PIK3CD gene, which encodes the catalytic p110δ subunit of phosphoinositide 3‐kinase δ (PI3Kδ), leading to hyperactivation of PI3Kδ and downstream Akt signaling with a consequent effect on immune cell development and differentiation.2, 3. This evidence concerns the gene PIK3CD and activated PI3K-delta syndrome.