AAL(S) is devoid of S1P agonism and has been utilised to promote the TTP-mediated activation of PP2A in A549 cells and inhibit pro-inflammatory cytokine production [32], AAL(S) has further been shown to retain the ability to activate PP2A in models of asthma and acute myeloid leukaemia [179–183]. This evidence concerns the gene ZFP36 and asthma.