Knockout studies demonstrate that Stk1 and VraS are not the targets of P2As. We tested the NTML library of MRSA mutants to identify potential pathways involved in P2A activity. In particular, we are interested in kinases like Stk1 and VraS, which are validated targets in the search for chemicals that synergize with β-lactams. stk1 and vraS knockout (k/o) or inactivation enhance the potency of cell wall-acting antibiotics, including β-lactams like oxacillin, against MRSA. Table shows us that P2As function even when stk1 and vraS are non-functional. Therefore, VraS and Stk1 are not the targets of P2As. Even though Stk1 and VraS are not involved, it was possible that other protein kinase-regulated pathways could facilitate penicillin G enhancement. So, we tested other kinase knockouts available in the NTML library. Surprisingly, we found multiple kinase knockouts abrogated the activity of 1. Many of these pathways facilitate antimicrobial resistance, but many are only known as metabolic regulators or else serve other functions (reviewed ) with no apparent connection with β-lactam or other resistance. This observation strongly suggests a global regulator, associated with multiple pathways, must be the target of P2As.