To begin to address this possibility, we used these previous data showing that sGCα1 pro-cancer functions are independent of NO signaling and sGCβ1 [7], [10] and that sGCβ1 can relieve sGCα1-mediated repression of p53 transcriptional activity [10], suggesting that sGCβ1 dimerization with sGCα1 can disrupt sGCα1 pro-cancer functions. Here, TP53 is linked to cancer.