During early infection, RSV engages a dual strategy: Suppression of extrinsic apoptosis via phosphoinositide 3-kinase (PI3K)–protein kinase B (Akt)–dependent up-regulation of cellular FLICE (FADD-like IL-1β–converting enzyme) inhibitory protein (cFLIP), and inhibition of N-GSDMD–driven pyroptosis through targeted degradation of zinc finger Asp-His-His-Cys-9 (ZDHHC9). This evidence concerns the gene AKT1 and infection.