Extracellular matrix (ECM) rigidity is a major effector of cell fate decisions. Whereas cell proliferation on stiff matrices, wherein Yes-associated protein (YAP) plays a pivotal role, is well documented, activation of apoptosis in response to soft matrices is poorly understood. Here, we show that YAP drives the apoptotic decision as well. We find that in cells on soft matrices, YAP is recruited to small adhesions, phosphorylated at the Y357 residue, and translocated into the nucleus, ultimately leading to apoptosis. In contrast, Y357 phosphorylation levels are dramatically low in large adhesions on stiff matrices. Furthermore, mild attenuation of actomyosin contractility allows adhesion growth on soft matrices, leading to reduced Y357 phosphorylation levels and resulting in cell growth. These findings indicate that failed adhesion reinforcement drives rigidity-dependent apoptosis through YAP and that this decision is not determined solely by ECM rigidity but rather by the balance between cellular forces and ECM rigidity. Display omitted •pYAP-Y357 accumulates at small adhesions on soft matrices and leads to apoptosis•YAP phosphorylation by c-Abl and Src drives the apoptotic decision•Failure of adhesion reinforcement determines pYAP-Y357 accumulation•Cellular decisions to undergo apoptosis or grow can be switched by myosin inhibition Shi et al. reveal that apoptosis on soft matrices depends on YAP Tyr357 phosphorylation and its accumulation in small adhesions, followed by its nuclear translocation. This process is blocked upon adhesion reinforcement on stiff matrices or via myosin inhibition on soft ones but is induced by myosin inhibition on stiff matrices.