Moreover, ZFP36L2 has been implicated in cell-cycle arrest [18], tumor necrosis factor-alpha (TNF-α) mRNA-destabilizing capability [13], B-cell development [19], skeletal muscle myogenesis [20], cancer progression [21], the regulation of mitochondrial fusion/fission during myocardial ischemia/reperfusion injury [22], and the negative regulation of TNF-α-induced CXCL8 (also known as interleukin 8, IL-8) in dermal fibroblasts [23]. This evidence concerns the gene TNF and myocardial ischemia.