Overall, elucidating the transient structural changes on the molecular organization of phospholipid interfaces induced by PLA2s in cell membranes should aid the design of basic peptides that suppress overactive endogenous PLA2s as seen in various autoimmune disorders and in chronic inflammatory conditions including rheumatoid arthritis, asthma, and possibly in some neurodegenerative diseases [18]. This evidence concerns the gene PLA2G2A and asthma.