For example, B2M could induce resistance to tipifarnib by inducing tumor cell survival, aggressiveness, and EMT via the induction of RAS-independent activation of the phosphoinositide 3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) and ERK signaling pathways [51, 52]. This evidence concerns the gene B2M and neoplasm.