In the case of cathepsin B, we report a strong implication of AtCathB1-2-3 in PCD induced by abiotic stress such as UV-C, oxidative stress (H2O2, MV) and ER stress, extending the role described for AtCathB1-2-3 in PCD induced by biotic stresses such as in HR caused by Pseudomonas infection.18 Putting together the inhibition of AtCathB by caspase-3 inhibitors and the genetic requirement of AtCathB for PCD, we propose that when caspase-3 inhibitors downregulate PCD in plants, they can do so by inhibiting cathepsin B that in turn blocks the PCD pathway at a point yet to be determined. The gene discussed is CASP3; the disease is Pseudomonas infection.