For this reason the development of new potential molecules that minimize the unfavorable effects and potentially allow dose reduction is absolutely needed and we believe inhibiting GRK2 is an attractive target not only because it can also normalize βAR signaling but also it appears to have exciting and novel non-GPCR effects that has appeal for targeting its inhibition that can synergize with β-blocker use in HF patients (see below). Here, ADRB2 is linked to hydrops fetalis.