Once arriving at alveolar space, membranous CD14 of ATRA-APL cells contributes to the phagocytic clearance of bacteria by binding with LPS on bacteria, and this also provokes the release of pro-inflammatory cytokines via the NF-κB signal transduction pathway to recruit more ATRA-APL cells from the blood stream into alveolar spaces for the development of DS in APL patients under induction ATRA treatment [16,20,22]. Here, NFKB1 is linked to Dravet syndrome.