For example, there is evidence of Cav1 involvement in the p38 mitogen-activated protein kinase (MAPK) signaling pathway, by which decreased Cav1-mediated activation of c-Jun N-terminal kinase (JNK), nuclear factor kappa B (NF-kB), and activator protein-1 (AP-1) leads to protection against inflammatory mechanisms in the setting of sepsis [47]. This evidence concerns the gene CAV1 and Sepsis.