The nucleotide-binding oligomerization domain, leucine-rich repeat, and pyrin domain-containing 3 (NLRP3) inflammasome are also believed to play a mechanistic role in the pathogenesis and severity of HF in animal and human studies [101] Subsequent studies using animal HF models (and models of other organ failure) have demonstrated decreased activation of NLRP3 independent of diabetes status, offering another potential mechanism for improving inflammation in HF with SGLT2 inhibition [102]. This evidence concerns the gene NLRP3 and hydrops fetalis.