These observations suggest that SMAD2 is located downstream of USP32 in GC, and USP32 could regulate the expression of SMAD2 and promote gastric carcinogenesis and cisplatin resistance by enhancing the stability of SMAD2 protein in gastric cancer cells, so targeting USP32 may be a potential therapeutic strategy for GC [25] (Fig. 6). Here, USP32 is linked to gastric cancer.