*4.5. Statistical Analyses*

Statistical analyses were carried out using GraphPad Prism 7. All cell death assays were subject to statistical analysis by two-way ANOVA and Bonferroni posttest. All cell death assays are the results of 3 independent experiments. Immunoblots presented are representative of 3 independent experiments.

**Supplementary Materials:** The following are available online at http://www.mdpi.com/2072-6651/11/8/450/s1, Figure S1: The combination of ricin/TRAIL induces caspase activation, Figure S2: Ricin/TNF-α and ricin/FasL do not induce caspase activation in A549 cells after 8 h, Figure S3: The apoptotic stimuli CHX/TRAIL, CHX/TNF-<sup>α</sup>, and CHX/FasL induce caspase cleavage, Figure S4: Ricin/TRAIL induces caspase cleavage that is prevented by pharmacologic inhibitors, Figure S5: A549 cell death by ricin/TNF-α and ricin/FasL does not depend on caspases-6 or -9, Figure S6: The apoptotic stimuli CHX/TNF-α and CHX/FasL induce Bax-dependent cell death, Figure S7: Cell death induced by ricin in combination with TNF-α or FasL does not depend on RIP1 kinase, Figure S8: Mcl1 protein loss does not di ffer between ricin/TRAIL, ricin/TNF-<sup>α</sup>, and ricin/FasL, Figure S9: Cell death induced by ricin/TNF-α and ricin/FasL does not depend on calpains or cathepsins L and K, Figure S10: The cathepsin inhibitor, CATI-1, has no e ffect on A549 cell death by ricin/TRAIL, Figure S11: Cell death induced by ricin/TNF-α or ricin/FasL is inhibited by N-acetylcysteine, Figure S12: Calu3 human lung epithelial cells are insensitive to cell death by ricin/TNF- or ricin/FasL, Figure S13: Calu3 human lung epithelial cells are insensitive to cell death by ricin/TNF-α or ricin/FasL,. Figure S14: Ricin/TRAIL induces caspase-dependent apoptosis while ricin/TNF-α and ricin/FasL induce cathepsin-dependent cell death in U937 human monocytes.

**Author Contributions:** Conceptualization, T.J.L. and N.J.M.; methodology, T.J.L. and W.D.M.; formal analysis, T.J.L., A.L.H., and C.G.K.; investigation, A.L.H., C.G.K., and C.A.P.; data curation, T.J.L.; writing—original draft preparation, T.J.L.; writing—review and editing, T.J.L., A.L.H., W.D.M., and N.J.M.; supervision, T.J.L. and W.D.M.; project administration, T.J.L.; funding acquisition, T.J.L, N.J.M.

**Funding:** This research was funded by the National Heart, Lung, and Blood Institute (NHLBI) of the National Institutes of Health (NIH), gran<sup>t</sup> number NIH R15-HL135675-01, awarded to T.J.L and the National Institutes of Allergy and Infectious Diseases (NIAID) of the NIH, contract number HHSN272201400021C, awarded to N.J.M. The content is solely the responsibility of the authors and does not necessarily represent the o fficial views of the NIH. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

**Conflicts of Interest:** The authors declare no conflict of interest.
