CD38 and neoplasm: The JAK/STAT3 cascade was mutated and aberrantly activated [10,66,67,68] in a number of lymphoid cancers, rendering cytokine-independent activation [69], immunosuppression- and tumor growth-related gene expressions (MCL1, SOX11, CD38, PD-L1, MUC1, MCL1, MYC and GTPase RhoU) [17,70,71,72,73,74,75,76], sustained tumor cell survival [71], prompted cell migration [76], differentiation advantage towards terminally differentiated B-cell lymphoma [77], resistance to cytotoxic and biological agents [74], disease progression [78] and shorter event-free survival [79].