Furthermore, multiple possible mechanisms may account for the anti-tumoral role of miR-125b, such as the following: (i) “miR-125b may enhance chromosomal stability by stimulating the expression of cohesin complex subunits (e.g., SMC2, SMC3, SMC4, STAG1, STAG2, SGO1, and PDS5B; referring to mRNA-Seq data)” (ii) “miR-125b may be transferred to tumor microenvironment via exosomes and inhibits TAM infiltration” (iii) “miR-125b may function through classical and/or nonclassical NF-kB signaling (e.g., RELB, NFKB2, and NFKBIA; referring to mRNA-Seq data)”. The gene discussed is NFKB1; the disease is neoplasm.