Besides the decreased inhibition of caspase-3 at 30 min after S. Heidelberg infection, there was not much evidence in the kinome peptide array results supporting the occurrence of increased cell death in HD11 cells at 30 min p.i. However, at the S. Heidelberg 2 h p.i. point, we observed an increase in positive regulation of apoptotic factors via the decreased activity of proteins involved in the inhibition of apoptosis, such as IkB-alpha (Y42), MNK1 (T255), caspase-3, and caspase-8, and the increased activity of proapoptotic factors like JNK1 and IRF1 (Table 4). The gene discussed is CASP3; the disease is infection.