Our findings suggest that the observed effect of FcγRIIIa on AR may not be the consequence of FcγRIIIa‐induced cell proliferation in AR‐expressing PCa cells, but rather due to that FcγRIIIa is functionally associated with AR and PIP5K1α associated pathways via protein–protein interactions. Here, PIP5K1A is linked to posterior cortical atrophy.