On the other hand, infected NLRP3-deficient macrophages treated with rapamycin did not affect either caspase-1 activation or processing/release of IL-1β by bacterial infection which trigger NLRC4 inflammasome (Figure S6), suggesting that PI3K-mediated signaling for autophagy is unassociated with the suppression of the NLRC4 inflammasome, consistent with the finding that VopQ induces PI3K-independent autophagy induction [24]. Here, NLRC4 is linked to bacterial infectious disease.