We then analyzed the Bcl2a1 cancer mutation sites for their: i) propensity to act as hub residues in the network, i.e., nodes that features a high degree of connectivity and likely to be important for the maintenance of the protein architecture or for communication throughout the network; ii) propensity to communicate to the BH3-binding region, estimating the shortest paths of communication between each mutation site and a group of residues (V48, R88, L52, V74, T91, and F95, Fig 6B), which we selected as hotspots for binding by the deep mutational scan discussed above (S1 Fig). Here, BCL2A1 is linked to cancer.