H2AX and pancreatic neoplasm: Early reports identified that Smad4‐knockdown human pancreatic cancer cells or mouse keratinocytes with Smad4 gene knockout exhibited increased spontaneous DNA damage and reduced DNA repair.[15, 31] Consistent with the genetic knockout mouse model, the protein levels of classical DNA damage markers, γ‐H2AX and RAD51, were markedly increased in Smad4KO cells (Figure S5B,C, Supporting Information).