Improved mOS outcomes from DEspR-inhibition presented here support two key emerging therapeutic paradigms in cancer: a) that reduction of feedforward dissemination-progression requires concurrent inhibition of both ends of the CSC/TC-plasticity spectrum and efficacy in the presence of CSC/TC-heterogeneity, i.e., with DEspR+/− CSCs and TCs [9, 10], and b) that stopping feedforward dissemination-progression in the permissive peritoneal space requires net reduction of pro-survival Mcl1 [31]. The gene discussed is MCL1; the disease is cancer.