We also established the hitherto undemonstrated tumor suppressor function of AnxA6 in TNBC cells, demonstrated that the reciprocal expression of AnxA6 and RasGRF2 is dependent on the modulation of Ca2+ influx by AnxA6 and that the contribution of AnxA6 in tumor cell growth and motility is at least in part, mediated by the effector functions of RasGRF2 i.e. activation of Ras proteins and inhibition of Cdc42 respectively. Here, CDC42 is linked to neoplasm.