In contrast to class IIa HDACs, class I HDACs have shown pro-hypertrophy effects via a variety of mechanisms, such as reducing autophagy through activation of mTOR signaling or suppressing the expression of Inpp5f (inositol polyphosphate-5-phosphatase f) and later inhibiting GSK3β (glycogen synthase kinase 3β) signaling, or inhibiting of DUSP5 (dual-specificity phosphatase 5) that negatively regulates ERK1/2-induced cardiac hypertrophy (39). Here, INPP5F is linked to cardiac hypertrophy.