The BM microenvironment can confer drug resistance through two major mechanisms (Figure 1(a)) [102]: (1) tumor cell adhesion, which involves MM cell binding to fibronectin, which in turn induces KIP1 and G1 growth arrest and confers cell-adhesion mediated drug resistance [103, 104] and (2) cytokine-mediated antiapoptotic sequelae, which involve the induction of JAK/STAT and PI3K/AKT signaling by cytokines in the BM microenvironment, which in turn mediates resistance to conventional and novel therapies. The gene discussed is AKT1; the disease is neoplasm.