CDKN2C and neoplasm: Clinical trials conducted by many research teams have shown that several molecular factors are also involved in disease progression and reduction of therapeutic success, including elevated levels of chromogranin A, overexpression of the mammalian target of rapamycin (mTOR), loss of expression of a cyclin-dependent inhibitor of CDKN1B kinases (p27) or the presence of 1 circulating tumor cell in 7.5 mL of blood (CTC-circulating tumor cells) [2,36,37,38].