Despite its efficacy, intrinsic and acquired resistance to irinotecan/SN38 is common and mechanistically heterogeneous [7], involving: TOP1 gene mutations [8], tumor cell stress responses to SN38‐TOP1‐DNA ternary complex [9, 10], activation of pro‐survival signaling pathways in cancer cells [11, 12] and epigenetic changes [13], etc. Here, TOP1 is linked to neoplasm.