Dysregulated neutrophils often accompany inflammatory processes of autoimmune diseases like epidermolysis bullosa acquisita (EBA). Previous work has shown that the PI3 kinase (PI3K) is a key molecule in the signaling pathway of neutrophils. Currently, four isoforms of the PI3K are known: PI3Kα, β, γ and δ which differ in their function and tissue distribution. We aim to investigate the role of these PI3K subunits in different features of neutrophils that can trigger disease pathogenesis, like the release of proteolytic and cytotoxic molecules and cytokines, the chemotactic activity, the viability and the ability to produce “neutrophil extracellular traps” (NETs) by using eight PI3K inhibitors, each in five different concentrations that vary in their specific binding side to the PI3K subunits.