CDKN2A and neoplasm: As shown in Fig. 7C, the tumors in the mice with miR-4256 agomir treatment grew more rapidly compared with the scrambled control; combined intratumoral injection of miR-4256 agomir and cholesterol-modified siHDAC5 partly eliminated the promoting effect of miR-4256 overexpression on tumor growth, while cointratumoral injection of miR-4256 agomir and cholesterol-modified siHDAC5 plus p16INK4a overexpression exhibited stronger tumor growth inhibition (Fig. 7C).