Previous studies showed that KAT2A regulates the cell cycle in pancreatic cancer cells through its succinylase function.[34] In our study, knockdown of KAT2A in the presence of TNF‐α reduced the succinylation level of VCP at K658, and this effect promoted mitophagy, inhibited OXPHOS, and suppressed the activation of BMMSC by TNF‐α, whereas the overexpression of KAT2A in the absence of TNF‐α led to the opposite results, suggesting that KAT2A mediates the activation of BMMSC by TNF‐α through its succinylase function. The gene discussed is TNF; the disease is pancreatic neoplasm.