NFKB1 and ischemia: STS further amplifies this pattern by increasing H2S and GSH levels in glial cells, suppressing TNF-α, IL-6, p38 MAPK, and NF-κB in a dose- and time-dependent manner [42], stimulating VEGF-mediated angiogenesis in ischemia [44], and, in our studies, demonstrating pH-dependent modulation of p53 via weak van der Waals interactions with Arg248, inducing conformational fluctuations without stable complex formation.