MCC950 continues to be suggested like a specific small molecule inhibitor that may selectively block NLRP3 inflammasome activation. However, the precise mechanism of their action continues to be ambiguous. Accumulating investigations imply chloride efflux-dependent ASC speck oligomerization and potassium efflux-dependent activation of caspase-1 would be the two relatively independent, but indispensable occasions for NLRP3 inflammasome activation. Previous studies recommended that influence of MCC950 on potassium efflux and it is consequent occasions for example interaction between NEK7 and NLRP3 are restricted. However, inhibiting chloride intracellular funnel-dependent chloride efflux results in a modification of inflammatory response, which has similarities towards the purpose of MCC950. According to these bits of information, we shed new insights around the knowledge of MCC950 that it is function might correlate with chloride efflux, chloride intracellular channels, or any other targets that act upstream of chloride efflux.