These findings could have broad clinical significance, as most solid tumors are known to have the following: (i) SC overpopulation that drives tumor development and growth, and (ii) inactivated APC that, by upregulating CYP26A1 expression and increasing ATRA degradation [108], could induce resistance to retinoids and reduce the effectiveness of retinoid therapies. The gene discussed is APC; the disease is neoplasm.