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These results demonstrate that TGF--induced transition from fibroblasts to myofibroblasts involves canonical TGF-/Smad2/3 signaling, non-canonical TGF-/ERK1/2 signaling, and ROS production via NAD(P)H oxidase

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Another study pointed out that pretreatment with 100 mg/kg NAC eliminated paclitaxel-induced allodynia in the CIPN mouse model, while in RAW264.7 cells, 50 mM NAC completely blocked the paclitaxel-induced release of high mobility group box 1 (HMGB1) and upregulation of CREB-binding protein (CBP) and p300/CBP-associated factor (PCAF) [63]