The reported observation that hnRNPA2 knockdown results in a p53-independent increase of p21 levels and an inhibition of cell proliferation [13], similar as observed here in ACCBMS1(p.R930H) fibroblasts, together with the results form the interaction analyses of the proteomic data that show the largest number of interactions to involve p21 and hnRNPA2B1 in ACC fibroblasts, suggest that the reduced protein levels of hnRNPA2B1 likely play a role in ACC pathogenesis. Here, CDKN1A is linked to adrenal cortex carcinoma.