MCL1 and pancreatic neoplasm: The basis for this potential, and the initiation of this study is that upregulation of antiapoptotic proteins, survivin [31–38], Mcl-1 [39–47], XIAP [35, 36, 38, 44, 48–55], and cIPA2 [55] are strongly involved in pancreatic cancer resistance, and that FL118 has been found to inhibit such gene expression in CRC and head-&-neck tumors [9].