The trick is to remember that the resting membrane potential settles near the equilibrium potential of whichever ion the membrane lets through most easily at rest.
At rest, the cell membrane is studded with open potassium "leak" channels, making it far more permeable to K$^+$ than to Na$^+$, Ca$^{2+}$ or Cl$^-$. Because K$^+$ permeability dominates, the resting voltage is pulled toward the potassium equilibrium potential calculated by the Nernst equation \[E_{K} = 61 \times \log_{10}\frac{[K^+]_{out}}{[K^+]_{in}} \approx -90 \text{ mV}\] which is why a typical RMP sits around $-70$ to $-90$ mV. A useful confirmation: changing extracellular K$^+$ shifts the RMP markedly (e.g. hyperkalaemia depolarises the cell), whereas altering extracellular Na$^+$ barely moves it.
The remaining ions play other roles: Na$^+$ rushing in produces the action-potential upstroke but contributes little at rest; Ca$^{2+}$ governs the plateau in cardiac cells and triggers release/contraction; Cl$^-$ mostly equilibrates passively and only modestly stabilises the potential.
So the ion that predominantly sets the resting membrane potential is potassium - option A.