Given that numerous endogenous agonists and sensitisers of TRPV4 are upregulated in sepsis, we hypothesised that blockade of TRPV4 activity using a pharmacological antagonist HC-067047, or genetic deletion of the channel (in global knockout mice) would be protective in a murine model of sepsis, attenuating the cardiovascular collapse associated with the development of septic shock. The gene discussed is TRPV4; the disease is Shock.